People living with resistant hypertension (RH) are at high risk of adverse cardiovascular events. The British and Irish Hypertension Society has identified suspected RH as a condition for which specialist guidance may improve rates of blood pressure control and help clinicians identify those individuals who may benefit from specialist review. In this position statement we provide a practical approach for the investigation and management of adults with RH. We highlight gaps in the current evidence and identify important future research questions. Our aim is to support the delivery of high-quality and consistent care to people living with RH across the UK and Ireland.

Resistant hypertension is a complex disorder that requires a comprehensive evaluation of several patient characteristics. Attention should be paid to medication and lifestyle adherence, and investigation into potential secondary causes of resistant hypertension should occur as clinically indicated. Moreover, a shared, multidisciplinary decision-making approach with the patient, specialized care providers, and family members may enhance blood pressure control.

Both blood pressure-lowering medication and sodium reduction are effective in hypertension control, but whether the effect of sodium reduction differ across blood pressure-lowering medications is unclear. This study aims to evaluate the dose-response effect of sodium intake reduction on blood pressure in treated hypertensive individuals and the impact of different classes of blood pressure-lowering drugs.

We searched multiple databases and reference lists up to July 9, 2024. Randomized controlled trials with a duration of ≥2 weeks comparing the effect of different levels of sodium intake (measured by 24-hour urinary sodium excretion) on blood pressure in hypertensive individuals treated with constant blood pressure-lowering medications were included. Instrumental variable meta-analyses based on random-effects models were conducted to evaluate the dose effect of sodium reduction on blood pressure. Subgroup analyses were performed based on the class of blood pressure-lowering drugs, age, baseline sodium and blood pressure levels, and study duration.

We included 35 studies (median duration of 28 days) with a total of 2885 participants. For every 100 mmol reduction in 24-hour urinary sodium excretion, systolic blood pressure decreased by 6.81 mm Hg (95% CI, 4.96-8.66), diastolic blood pressure decreased by 3.85 mm Hg (95% CI, 2.26-5.43), and mean arterial pressure decreased by 4.83 mm Hg (95% CI, 3.22-6.44). The dose-response effects varied across classes of blood pressure-lowering medications, with greater effects observed in the β-blockers, renin-angiotensin-aldosterone system inhibitors, and dual therapy groups. No significant subgroup differences were observed across subgroups defined by age, baseline 24-hour urinary sodium excretion, blood pressure levels, or study duration.

Pooled evidence suggests a dose-response relationship between sodium reduction and blood pressure in treated individuals with hypertension, influenced by the class of blood pressure-lowering medications.

The relationship between dietary inflammation index (DII) and the risk of hypertension is inconsistent across published epidemiological studies. This meta-analysis aimed to investigate the dose-response relationship between DII score and the risk of hypertension. A systematic search for relevant studies was conducted in PubMed, Web of Science, and Embase databases until January 9, 2024. After data extraction, the summarized relative risks (RRs) and 95% confidence intervals (95% CIs) were estimated using the Der Simonian and Laird random effect model, and dose-response analyses were performed using restricted cubic splines. A total of six studies with 120,294 participants and 36,725 cases of hypertension were included. The pooled relative risk (RR) for hypertension risk was 1.15 (95% CI: 1.06, 1.26) for the highest DII score compared with the lowest, and 1.10 (95% CI: 1.03, 1.18) for higher DII score compared with the lower. The dose-response meta-analysis further demonstrated a positive association between elevated DII scores and hypertension risk. For each one-unit increase in the DII score, the incidence of hypertension increased by 4% (RR = 1.04, 95% CI: 1.00, 1.07). Pro-inflammation dietary increases the risk of hypertension. Therefore, reducing pro-inflammatory components in the diet may be beneficial for the prevention and control of hypertension.

Minerals play an important role in human health, but their effect on urinary function remains controversial. The aim of this study was to assess the association between dietary intake of minerals (Ca, P, Mg, Fe, Zn, Cu, Na, K, Se) and urine flow rate (UFR).

We conducted a cross-sectional study using the National Health and Nutrition Examination Survey (NHANES, 2009-2018) database. Multivariate regression and smooth curve fitting were used to investigate the association between dietary mineral intakes and UFR. Subgroup analyses and interaction tests were used to investigate whether this association was stable in the population.

Our study involving 10,229 representative adult NHANES participants showed an association between Mg intake and UFR in a linear regression model for continuous variables. And in the model analysis of tertile categorical variables, we observed a positive association between six mineral intakes (Ca, Mg, Zn, Cu, Na, and K) and UFR. Smoothed curve fitting and threshold effect analysis further support the nonlinear relationship between mineral intakes and UFR. Subgroup analyses and interaction tests ensured the reliability and robustness of the findings.

This study examined the effects of nine dietary minerals on UFR and found that intake of Ca, Mg, Zn, Cu, Na, and K were positively correlated with UFR, suggesting that these minerals may have a positive effect on improving urinary function. In particular, Mg showed a more significant positive correlation with UFR in women, while Na showed a stronger positive correlation in diabetics. However, P, Fe and Se did not show significant correlations. In summary, although these findings provide a preliminary understanding of the relationship between dietary minerals and urinary function, further prospective studies are still necessary to validate these relationships and explore the physiologic mechanisms underlying them.

Resistant hypertension (RH) includes hypertensive patients with uncontrolled blood pressure (BP) while receiving ≥3 BP-lowering medications or with controlled BP while receiving ≥4 BP-lowering medications. The exact prevalence of RH is challenging to quantify. However, a reasonable estimate of true RH is around 5% of the hypertensive population. Patients with RH have higher cardiovascular risk as compared with hypertensive patients in general. Standardized office BP measurement, confirmation of medical adherence, search for drug- or substance-induced BP elevation, and ambulatory or home BP monitoring are mandatory to exclude pseudoresistance. Appropriate further investigations, guided by clinical data, should be pursued to exclude possible secondary causes of hypertension. The management of RH includes the intensification of lifestyle interventions and the modification of antihypertensive drug regimens. The essential aspects of lifestyle modification include sodium restriction, body weight control, regular exercise, and healthy sleep. Step-by-step adjustment of the BP-lowering drugs based on the available evidence is proposed. The suitable choice of diuretics according to patients' renal function is presented. Sacubitril/valsartan can be carefully substituted for the prior renin-angiotensin system blockers, especially in those with heart failure with preserved ejection fraction. If BP remains uncontrolled, device therapy such as renal nerve denervation should be considered. Since device-based treatment is an invasive and costly procedure, it should be used only after careful and appropriate case selection. In real-world practice, the management of RH should be individualized depending on each patient's characteristics.

Secondary hypertension in the elderly poses many challenges and requires a comprehensive diagnostic and management approach. This review explores the prevalence, diagnostic strategies, and treatment modalities for secondary hypertension in elderly patients, focusing on etiologies including primary aldosteronism, renal vascular disease, renal parenchymal disease, obstructive sleep apnea, thyroid disorders, Cushing's syndrome, pheochromocytomas and paragangliomas, and drug-induced hypertension. Key considerations include age-related changes in physiology and atypical presentations of underlying conditions necessitating thorough screening with a combination of clinical evaluation, laboratory tests, and imaging studies. Collaboration among healthcare providers is essential to ensure a timely diagnosis and personalized management tailored to the unique needs of elderly patients. Further research is needed to address knowledge gaps and optimize clinical strategies for managing secondary hypertension in this population.

Background Hypertension (HTN) is a global health issue as it causes significant mortality and morbidity among the worldwide population. Various treatments are available, but many patients are unable to control the disease. There are various factors like medication non-adherence and lifestyle habits that contribute to this problem. There is a need for evidence-based interventions to address HTN effectively, especially in regions like Saudi Arabia, where there is limited data on uncontrolled HTN. This study aimed to assess the prevalence of uncontrolled HTN and contributing factors to poor blood pressure control among patients in Primary Health Centers (PHCs) in Riyadh, Saudi Arabia. Methodology An analytical cross-sectional study was conducted using an interviewer-administered questionnaire among all patients aged 18 years and above who have uncontrolled HTN and who visited the PHCs of Riyadh's first health cluster in Saudi Arabia. Data was cleaned in Microsoft Excel and analyzed using IBM SPSS 29. Results The study comprised 516 patients with HTN. The majority were males (53.1%, n=274) compared to females (46.9%, n=242), with an average age of 58 years (SD=10.5). Notably, most patients were obese (63.2%, n=326), and 62.4% (n=322) had uncontrolled HTN. Multivariate analysis identified sociodemographic factors like higher education (p-value = 0.013, adjusted odds ratio (AOR) = 0.795) as protective against uncontrolled HTN, while employment (p-value = 0.031, AOR = 1.786) increased the risk of uncontrolled HTN. Risk factors such as smoking (p-value = 0.001, AOR = 3.011) and salt restriction (p-value = 0.021, AOR = 0.643) significantly influenced HTN control. Management-related predictors like stopping medication after feeling better (p-value = 0.001, AOR = 3.196) were also found significant. Conclusion This study revealed a high prevalence of uncontrolled HTN, especially among males and obese individuals. Sociodemographic factors like higher education were protective, while employment increased the risk of the disease. Further, smoking, salt restriction, and medication adherence significantly impacted HTN control, highlighting the importance of tailored interventions.

Several observational studies have been conducted to assess the prevalence of cardiovascular risk factors in hypertensive patients; however, none has yet investigated prevalence, clustering, and current management of cardiovascular risk factors upon first referral to hypertension specialists, which is the aim of the present study.

Consecutive adult outpatients with essential/secondary hypertension were included at the time of their first referral to hypertension specialists at 13 Italian centers in the period April 2022-2023 if they had at least one additional major cardiovascular risk factor among LDL-hypercholesterolemia, type 2 diabetes, and cigarette smoking. Prevalence, degree of control, and current management strategies of cardiovascular risk factors were assessed.

A total of 255 individuals were included, 40.2% women and 98.4% Caucasian. Mean age was 60.3±13.3 years and mean blood pressure [BP] was 140.3±17.9/84.8±12.3 mmHg). Most participants were smokers (55.3%), had a sedentary lifestyle (75.7%), suffered from overweight/obesity (51%) or high LDL-cholesterol (41.6%), had never adopted strategies to lose weight (55.7%), and were not on a low-salt diet (57.4%). Only a minority of patients reported receiving specialist counseling, and 27.9% had never received recommendations to correct unhealthy lifestyle habits. Nearly 90% of individuals with an estimated high/very high cardiovascular risk profile did not achieve recommended LDL-cholesterol targets.

In patients with hypertension, both pharmacological and lifestyle therapeutic advice are yet to improve before referral to hypertension specialists. This should be considered in the primary care setting in order to optimize cardiovascular risk management strategies.

Resistant hypertension is defined as blood pressure that remains above the therapeutic goal despite concurrent use of at least three antihypertensive agents of different classes, including a diuretic, with all agents administered at maximum or maximally tolerated doses. Resistant hypertension is also diagnosed if blood pressure control requires four or more antihypertensive drugs. Assessment requires the exclusion of apparent treatment resistant hypertension, which is most often the result of non-adherence to treatment. Resistant hypertension is associated with major cardiovascular events in the short and long term, including heart failure, ischemic heart disease, stroke, and renal failure. Guidelines from several professional organizations recommend lifestyle modification and antihypertensive drugs. Medications typically include an angiotensin converting enzyme inhibitor or angiotensin receptor blocker, a calcium channel blocker, and a long acting thiazide-type/like diuretic; if a fourth drug is needed, evidence supports addition of a mineralocorticoid receptor antagonist. After a long pause since 2007 when the last antihypertensive class was approved, several novel agents are now under active development. Some of these may provide potent blood pressure lowering in broad groups of patients, such as aldosterone synthase inhibitors and dual endothelin receptor antagonists, whereas others may provide benefit by allowing treatment of resistant hypertension in special populations, such as non-steroidal mineralocorticoid receptor antagonists in patients with chronic kidney disease. Several device based approaches have been tested, with renal denervation being the best supported and only approved interventional device treatment for resistant hypertension.

Resistant hypertension (RH) is defined as systolic blood pressure (SBP) or diastolic blood pressure (DBP) that remains .140 mmHg or .90 mmHg, respectively, despite an appropriate lifestyle and the use of optimal or maximally tolerated doses of a three-drug combination, including a diuretic. This definition encompasses the category of controlled RH, defined as the presence of blood pressure (BP) effectively controlled by four or more antihypertensive agents, as well as refractory hypertension, referred to as uncontrolled BP despite five or more drugs of different classes, including a diuretic. To confirm RH presence, various causes of pseudo-resistant hypertension (such as improper BP measurement techniques and poor medication adherence) and secondary hypertension must be ruled out. Inadequate BP control should be confirmed by out-of-office BP measurement. RH affects about 5% of the hypertensive population and is associated with increased cardiovascular morbidity and mortality. Once RH presence is confirmed, patient evaluation includes identification of contributing factors such as lifestyle issues or interfering drugs/substances and assessment of hypertension-mediated organ damage. Management of RH comprises lifestyle interventions and optimisation of current medication therapy. Additional drugs should be introduced sequentially if BP remains uncontrolled and renal denervation can be considered as an additional treatment option. However, achieving optimal BP control remains challenging in this setting. This review aims to provide an overview of RH, including its epidemiology, pathophysiology, diagnostic work-up, as well as the latest therapeutic developments.

The previous studies that examined the effectiveness of unsupervised machine learning methods versus traditional methods in assessing dietary patterns and their association with incident hypertension showed contradictory results. Consequently, our aim is to explore the correlation between the incidence of hypertension and overall dietary patterns that were extracted using unsupervised machine learning techniques.

Data were obtained from Japanese male participants enrolled in a prospective cohort study between August 2008 and August 2010. A final dataset of 447 male participants was used for analysis. Dimension reduction using uniform manifold approximation and projection (UMAP) and subsequent K-means clustering was used to derive dietary patterns. In addition, multivariable logistic regression was used to evaluate the association between dietary patterns and the incidence of hypertension.

We identified four dietary patterns: 'Low-protein/fiber High-sugar,' 'Dairy/vegetable-based,' 'Meat-based,' and 'Seafood and Alcohol.' Compared with 'Seafood and Alcohol' as a reference, the protective dietary patterns for hypertension were 'Dairy/vegetable-based' (OR 0.39, 95% CI 0.19-0.80, P = 0.013) and the 'Meat-based' (OR 0.37, 95% CI 0.16-0.86, P = 0.022) after adjusting for potential confounding factors, including age, body mass index, smoking, education, physical activity, dyslipidemia, and diabetes. An age-matched sensitivity analysis confirmed this finding.

This study finds that relative to the 'Seafood and Alcohol' pattern, the 'Dairy/vegetable-based' and 'Meat-based' dietary patterns are associated with a lower risk of hypertension among men.

The term RH describes a subgroup of hypertensive patients whose BP is uncontrolled despite the use of at least three antihypertensive drugs in an appropriate combination at optimal or best tolerated doses. True RH is considered when appropriate lifestyle measures and treatment with optimal or best tolerated doses of three or more drugs (a thiazide/thiazide-like diuretic, plus renin-angiotensin system -RAS- blocker and a calcium channel blocker -CCB-) fail to lower office BP to <140/90 mmHg; besides the inadequate BP control should be confirmed by home blood pressure monitoring (HBPM) or 24-hour ambulatory; and evidence of adherence to therapy and exclusion of secondary causes of hypertension are required. RH patients are at a high risk of cardiovascular events and death. RH is associated with a higher prevalence of end-organ damage. When stricter criteria are applied, a reasonable estimate of the prevalence of true RH is 5 % of the total hypertensive population. The predominant hemodynamic pattern appears to be increased systemic vascular resistance and plasma volume with normal or even low cardiac output. We must rule out pseudo-resistance before diagnosing true drug resistance. RH is a therapeutic challenge, and its management includes lifestyle interventions, avoiding nonadherence to treatment, avoiding inertia, appropriate use of antihypertensive drugs based on current evidence, especially long-acting diuretics, and the addition of mineralocorticoid receptor antagonists. RCTs to identify the most protective medical therapy in RH are needed. A series of drugs in different stages of investigation could significantly impact RH treatment in the future.

Patients with resistant hypertension are the group of hypertensive patients with the highest cardiovascular risk.

All rules and guidelines for treatment of hypertension should be followed strictly to obtain blood pressure (BP) control in resistant hypertension. The mainstay of treatment of hypertension, also for resistant hypertension, is pharmacological treatment, which should be tailored to each patient's specific phenotype. Therefore, it is pivotal to assess nonadherence to pharmacological treatment as this remains the most challenging problem to investigate and manage in the setting of resistant hypertension.

Once adherence has been confirmed, patients must be thoroughly worked-up for secondary causes of hypertension. Until such possible specific causes have been clarified, the diagnosis is apparent treatment-resistant hypertension (TRH). Surprisingly few patients remain with true TRH when the various secondary causes and adherence problems have been detected and resolved. Refractory hypertension is a term used to characterize the treatment resistance in hypertensive patients using ≥5 antihypertensive drugs. All pressor mechanisms may then need blockage before their BPs are reasonably controlled.

Patients with resistant hypertension need careful and sustained follow-up and review of their medications and dosages at each term since medication adherence is a very dynamic process.

Patients with treatment resistant hypertension (TRH) are known to have elevated sodium (Na) content in muscle and skin. Renal denervation (RDN) emerged as an adjacent therapeutic option in this group of patients. This analysis aimed at evaluating whether tissue Na content predicts blood pressure (BP) response after RDN in patients with TRH. Radiofrequency-device based RDN was performed in 58 patients with uncontrolled TRH. Office and 24-h ambulatory BP were measured at baseline and after 6 months. To assess tissue Na content Na magnetic resonance imaging (Na-MRI) was performed at baseline prior to RDN. We splitted the study cohort into responders and non-responders based on the median of systolic 24-h ambulatory blood pressure (ABP) reduction after 6 months and evaluated the association between BP response to RDN and tissue Na content in skin and muscle. The study was registered at http://www.clinicaltrials.gov (NCT01687725). Six months after RDN 24-h ABP decreased by -8.6/-4.7 mmHg. BP-Responders were characterized by the following parameters: low tissue sodium content in the skin (p = 0.040), female gender (p = 0.027), intake of aldosterone antagonists (p = 0.032), high baseline 24-h night-time heart rate (p = 0.045) and high LDL cholesterol (p < 0.001). These results remained significant after adjustment for baseline 24-h systolic BP. Similar results were obtained when the median of day-time and night-time ABP reduction after 6 months were used as cut-off criteria for defining BP response to RDN. We conclude that in addition to clinical factors including baseline 24-h ABP Na-MRI may assist to select patients with uncontrolled TRH for RDN treatment.

Resistant hypertension (RH) is a severe form of hypertension associated with increased cardiovascular risk. Although true RH affects less than 10% of the patients receiving antihypertensive therapy, the absolute number is high and continues to increase. The workup of these patients requires screening for secondary hypertension and pseudoresistance, including poor adherence to prescribed medicines and the white-coat phenomenon. The treatment of RH consists of lifestyle modifications and pharmacological therapies. Lifestyle modifications include dietary adjustments, weight loss, physical activity, and limiting alcohol consumption; pharmacological therapies include diuretics, mineralocorticoid receptor antagonists, beta blockers, angiotensin receptor-neprilysin inhibitors, and others. Over the last 15 years, interventional approaches have emerged as adjunct treatment options; we highlight catheter-based renal denervation. This review summarizes the rationales and latest clinical evidence and, based thereon, proposes an updated algorithm for the management of RH.

A comprehensive pathophysiological mechanism to explain the relationship between high-salt intake and hypertension remains undefined. Evidence suggests that chloride, as the accompanying anion of sodium in dietary salt, is necessary to develop hypertension. We evaluated whether reducing dietary Cl- while keeping a standard Na+ intake modified blood pressure, cardiac hypertrophy, renal function, and vascular contractility after angiotensin II (AngII) infusion.

C56BL/6J mice fed with standard Cl- diet or a low-Cl- diet (equimolar substitution of Cl- by a mixture of Na+ salts, both diets with standard Na+ content) received AngII (infusion of 1.5 mg/kg/day) or vehicle for 14 days. We measured systolic blood pressure (SBP), glomerular filtration rate (GFR), natriuretic response to acute saline load, and contractility of aortic rings from mice infused with vehicle and AngII, in standard and low-Cl- diet.

The mice fed the standard diet presented increased SBP and cardiac hypertrophy after AngII infusion. In contrast, low-Cl- diet prevented the increase of SBP and cardiac hypertrophy. AngII-infused mice fed a standard diet presented hampered natriuretic response to saline load, meanwhile the low-Cl- diet preserved natriuretic response in AngII-infused mice, without change in GFR. Aortic rings from mice fed with standard diet or low-Cl- diet and infused with AngII presented a similar contractile response.

We conclude that the reduction in dietary Cl- as the accompanying anion of sodium in salt is protective from AngII pro-hypertensive actions due to a beneficial effect on kidney function and preserved natriuresis.

Incorporating aggressive lifestyle modifications along with antihypertensive medication therapy is a crucial treatment strategy to enhance the control rate of hypertension. Dietary modification is one of the important lifestyle interventions for hypertension, and it has been proven to have a clear effect. Among food ingredients, sodium and potassium have been found to have the strongest association with blood pressure. The blood pressure-lowering effect of a low sodium diet and a high potassium diet has been well established, especially in hypertensive population. A high intake of potassium, a key component of the Dietary Approaches to Stop Hypertension (DASH) diet, has also shown a favorable impact on the risk of cardiovascular events. Additionally, research conducted with robust measurement methods has shown cardiovascular benefits of low-sodium intake. In this review, we aim to discuss the evidence regarding the relationship between the low sodium and high potassium diet and blood pressure and cardiovascular events.

A causal relationship exists between salt intake and hypertension, stroke, and kidney disease. However, whether or not reduced salt intake slows progression of renal diseases has been intensely debated.

In this prospective, open-label, randomized controlled trial, we examined the impact of a low salt diet on renal function, blood pressure, and other metabolic parameters. Herein, 194 patients with chronic kidney disease (CKD) stages 1 to 3 were randomized in low salt (intervention) and control groups. The intervention group was provided a low salt diet (1.5 g/day) for 3 months. The control group consumed their usual diet, and daily food intake was recorded in the control group. Renal function tests, 24-h urinary sodium excretion, urinary protein, serum calcium, phosphorus, and electrolyte levels were recorded monthly.

After 3 months, the mean reduction in estimated glomerular filtration rate was significantly higher in the control group (mean reduction in eGFR, -3.011 mL/min/1.73 m2; 95% confidence interval (CI) = -5.367, -0.656, P = .013). Blood pressure (BP) decreased significantly in both groups; systolic and diastolic BP reduction at 3 months was significantly greater in the intervention group (systolic BP mean reduction -6.57/-4.29 mmHg; 95% CI = -10.24, -2.89) and diastolic BP mean reduction -6.95, -1.64 mmHg) compared with the control group (systolic BP mean reduction -0.58/-2.63 mmHg; 95%, CI = -4.33, 3.17 and diastolic BP mean reduction -5.34, -0.08 mmHg). The mean reduction in 24-h urine sodium excretion was greater in the intervention group, reaching a significant level at month 2 (-14.45 mmol/day; 95% CI = -27.63, -1.22).

Overall, salt restriction can help slow the progression of renal insufficiency and results in statistically significant and clinically important reductions in BP among patients with CKD.

NCT05716386 on 28/01/2023.

Dietary sodium recommendations are debated partly due to variable blood pressure (BP) response to sodium intake. Furthermore, the BP effect of dietary sodium among individuals taking antihypertensive medications is understudied.

To examine the distribution of within-individual BP response to dietary sodium, the difference in BP between individuals allocated to consume a high- or low-sodium diet first, and whether these varied according to baseline BP and antihypertensive medication use.

Prospectively allocated diet order with crossover in community-based participants enrolled between April 2021 and February 2023 in 2 US cities. A total of 213 individuals aged 50 to 75 years, including those with normotension (25%), controlled hypertension (20%), uncontrolled hypertension (31%), and untreated hypertension (25%), attended a baseline visit while consuming their usual diet, then completed 1-week high- and low-sodium diets.

High-sodium (approximately 2200 mg sodium added daily to usual diet) and low-sodium (approximately 500 mg daily total) diets.

Average 24-hour ambulatory systolic and diastolic BP, mean arterial pressure, and pulse pressure.

Among the 213 participants who completed both high- and low-sodium diet visits, the median age was 61 years, 65% were female and 64% were Black. While consuming usual, high-sodium, and low-sodium diets, participants' median systolic BP measures were 125, 126, and 119 mm Hg, respectively. The median within-individual change in mean arterial pressure between high- and low-sodium diets was 4 mm Hg (IQR, 0-8 mm Hg; P < .001), which did not significantly differ by hypertension status. Compared with the high-sodium diet, the low-sodium diet induced a decline in mean arterial pressure in 73.4% of individuals. The commonly used threshold of a 5 mm Hg or greater decline in mean arterial pressure between a high-sodium and a low-sodium diet classified 46% of individuals as "salt sensitive." At the end of the first dietary intervention week, the mean systolic BP difference between individuals allocated to a high-sodium vs a low-sodium diet was 8 mm Hg (95% CI, 4-11 mm Hg; P < .001), which was mostly similar across subgroups of age, sex, race, hypertension, baseline BP, diabetes, and body mass index. Adverse events were mild, reported by 9.9% and 8.0% of individuals while consuming the high- and low-sodium diets, respectively.

Dietary sodium reduction significantly lowered BP in the majority of middle-aged to elderly adults. The decline in BP from a high- to low-sodium diet was independent of hypertension status and antihypertensive medication use, was generally consistent across subgroups, and did not result in excess adverse events.

ClinicalTrials.gov Identifier: NCT04258332.

High sodium intake is an accepted risk factor for hypertension, while low Na⁺ intake has also been associated with increased risk of cardiovascular events. In this cross-sectional study, we examined the association of 24-h urinary Na⁺ excretion with haemodynamics and volume status.

Haemodynamics were recorded in 510 normotensive and never-treated hypertensive subjects using whole-body impedance cardiography and tonometric radial artery pulse wave analysis. The results were examined in sex-specific tertiles of 24-h Na⁺ excretion, and comparisons between normotensive and hypertensive participants were also performed. Regression analysis was used to investigate factors associated with volume status. The findings were additionally compared to 28 patients with primary aldosteronism.

The mean values of 24-h urinary Na⁺ excretion in tertiles of the 510 participants were 94, 148 and 218 mmol, respectively. Average tertile age (43.4-44.7 years), office blood pressure and pulse wave velocity were corresponding in the tertiles. Plasma electrolytes, lipids, vitamin D metabolites, parathyroid hormone, renin activity, aldosterone, creatinine and insulin sensitivity did not differ in the tertiles. In supine laboratory recordings, there were no differences in aortic systolic and diastolic blood pressure, heart rate, cardiac output and systemic vascular resistance. Extracellular water volume was higher in the highest versus lowest tertile of Na⁺ excretion. In regression analysis, body surface area and 24-h Na⁺ excretion were independent explanatory variables for extracellular water volume. No differences in urine Na⁺ excretion and extracellular water volume were found between normotensive and hypertensive participants. When compared with the 510 participants, patients with primary aldosteronism had 6.0% excess in extracellular water (p = .003), and 24-h Na⁺ excretion was not related with extracellular water volume.

In the absence of mineralocorticoid excess, Na⁺ intake, as evaluated from 24-h Na⁺ excretion, predominantly influences extracellular water volume without a clear effect on blood pressure.

The current review is to describe the definition and prevalence of resistant arterial hypertension (RAH), the difference between refractory hypertension, patient characteristics and major risk factors for RAH, how RAH is diagnosed, prognosis and outcomes for patients.

According to the WHO, approximately 1.28 billion adults aged 30-79 worldwide have arterial hypertension, and over 80% of them do not have blood pressure (BP) under control. RAH is defined as above-goal elevated BP despite the concurrent use of 3 or more classes of antihypertensive drugs, commonly including a long-acting calcium channel blocker, an inhibitor of the renin-angiotensin system (angiotensin-converting enzyme inhibitor or angiotensin receptor blocker), and a thiazide diuretic administered at maximum or maximally tolerated doses and at appropriate dosing frequency. RAH occurs in nearly 1 of 6 hypertensive patients. It often remains unrecognised mainly because patients are not prescribed ≥3 drugs at maximal doses despite uncontrolled BP.

RAH distinctly increases the risk of developing coronary artery disease, heart failure, stroke and chronic kidney disease and confers higher rates of major adverse cardiovascular events as well as increased all-cause mortality. Timely diagnosis and treatment of RAH may mitigate the associated risks and improve short and long-term prognosis.

To provide an update and review approaches to the treatment of resistant hypertension (RH) with a focus on emerging potential therapies.

Resistant hypertension is defined as a blood pressure that remains elevated above a patient's individualized target despite the concurrent use of 3 antihypertensive agents of different classes including a diuretic or use of 4 or more antihypertensive agents. Patients with RH have an increased risk of adverse cardiovascular and renal outcomes. Most RH is attributed to apparent RH and is not true RH. True RH is a diagnosis of exclusion after apparent RH has been excluded. Treatment of RH is challenging, and blood pressure goal is often difficult to achieve. Currently several new therapies have emerged with forthcoming data that provide promise for improved blood pressure control in those with resistant hypertension. Once RH has been diagnosed, patients should be on standardized therapy that includes agents from three different classes including a diuretic with addition in most cases of a mineralocorticoid as a fourth line agent. There are newer agents in development currently being studied in clinical trials including dual endothelin receptor antagonists and aldosterone synthase inhibitors that appear to be efficacious. Other approved medications including SGLT2 inhibitors and non-steroidal mineralocorticoids such as finerenone also need to be incorporated into treatment paradigms. Renal denervation with catheter based devices is another potential promising treatment option in this population.

Although reports vary, the prevalence of true resistant hypertension and apparent treatment-resistant hypertension (aTRH) has been reported to be 10.3% and 14.7%, respectively. As there is a rapid increase in the prevalence of obesity, chronic kidney disease, and diabetes mellitus, factors that are associated with resistant hypertension, the prevalence of resistant hypertension is expected to rise as well. Frequently, patients with aTRH have pseudoresistant hypertension [aTRH due to white-coat uncontrolled hypertension (WUCH), drug underdosing, poor adherence, and inaccurate office blood pressure (BP) measurements]. As the prevalence of WUCH is high among patients with aTRH, the use of out-of-office BP measurements, both ambulatory blood pressure monitoring (ABPM) and home blood pressure monitoring (HBPM), is essential to exclude WUCH. Non-adherence is especially problematic, and methods to assess adherence remain limited and often not clinically feasible. Therefore, the use of HBPM and higher utilization of single-pill fixed-dose combination treatments should be emphasized to improve drug adherence. In addition, primary aldosteronism and symptomatic obstructive sleep apnea are quite common in patients with hypertension and more so in patients with resistant hypertension. Screening for these diseases is essential, as the treatment of these secondary causes may help control BP in patients who are otherwise difficult to treat. Finally, a proper drug regimen combined with lifestyle modifications is essential to control BP in these patients.

Approximately 10% of the adults with hypertension fail to achieve the recommended blood pressure treatment targets on 3 antihypertensive medications or require ≥ 4 medications to achieve goal. These patients with 'resistant hypertension' have an increased risk of target organ damage, adverse clinical events, and all-cause mortality. Although lifestyle modification is widely recommended as a first-line approach for the management of high blood pressure, the effects of lifestyle modifications in patients with resistant hypertension has not been widely studied. This review aims to provide an overview of the emerging evidence on the benefits of lifestyle modifications in patients with resistant hypertension, reviews potential mechanisms by which lifestyles may reduce blood pressure, and discusses the clinical implications of the recent findings in this field.

Evidence from single-component randomized clinical trials demonstrated that aerobic exercise, weight loss and dietary modification can reduce clinic and ambulatory blood pressure in patients with resistant hypertension. Moreover, evidence from multi-component trials involving exercise and dietary modification and weight management can facilitate lifestyle change, reduce clinic and ambulatory blood pressure, and improve biomarkers of cardiovascular risk. This new evidence supports the efficacy of lifestyle modifications added to optimized medical therapy in reducing blood pressure and improving cardiovascular risk biomarkers in patients with resistant hypertension. These findings need to be confirmed in larger studies, and the persistence of benefit over extended follow-up needs further study.

Resistant hypertension (RHT) is typically defined as blood pressure that remains above guideline-directed targets despite the use of three anti-hypertensives, usually including a diuretic, at optimal or maximally tolerated doses. It is generally estimated to affect 10-30% of those diagnosed with hypertension, though the true incidence might be lower after one factor in the prevalence of non-adherence. Risk factors for its development include diabetes, obesity and other adverse lifestyle factors, and a diagnosis of RHT confers a greater risk of adverse cardiovascular outcomes, such as stroke, heart failure and mortality. It is essential to exclude pseudoresistance and secondary hypertension and to ensure non-pharmacologic management is optimised prior to consideration of fourth-line anti-hypertensive agents or advanced interventions, such as device therapies. In this review, we will cover the different definitions of RHT, along with the importance of careful diagnosis and management strategies, and discuss newer agents and research needs.

Patients with treatment resistant hypertension (TRH) are at particular risk of cardiovascular disease. Life style modification, including sodium restriction, is an important part of the treatment of these patients. We aimed to analyse if self-performed dietary sodium restriction could be implemented in patients with TRH and to evaluate the effect of this intervention on blood pressure (BP). Moreover, we aimed to examine if mechanisms involving nitric oxide, body water content and BNP, renal function and handling of sodium were involved in the effect on nocturnal and 24-h BP. Also, measurement of erythrocyte sodium sensitivity was included as a possible predictor for the effect of sodium restriction on BP levels.

TRH patients were included for this interventional four week study: two weeks on usual diet and two weeks on self-performed sodium restricted diet with supplementary handed out sodium-free bread. At the end of each period, 24-h BP and 24-h urine collections (sodium, potassium, ENaC) were performed, blood samples (BNP, NOx, salt blood test) were drawn, and bio impedance measurements were made.

Fifteen patients, 11 males, with a mean age of 59 years were included. After sodium restriction, urinary sodium excretion decreased from 186 (70) to 91 [51] mmol/24-h, and all but one reduced sodium excretion. Nocturnal and 24-h systolic BP were significantly reduced (- 8 and - 10 mmHg, respectively, p < 0.05). NOx increased, BNP and extracellular water content decreased, all significantly. Change in NOx correlated to the change in 24-h systolic BP. BP response after sodium restriction was not related to sodium sensitivity examined by salt blood test.

Self-performed dietary sodium restriction was feasible in a population of patients with TRH, and BP was significantly reduced. Increased NOx synthesis may be involved in the BP lowering effect of sodium restriction.

The study was registered in Clinical trials with ID: NCT06022133.

Hypertensive nephropathy is characterized by long-term damage to renal tissues by chronic uncontrolled hypertension, and ultimately leads to the development of renal fibrosis. The epithelial-mesenchymal transition (EMT) potentially contributes to the promotion of renal fibrosis in chronic kidney disease (CKD). In this study, we investigated the potential roles of canagliflozin (Cana) on renal EMT and oxidative stress through its effects on sirtuin 3 (SIRT3) expression. High-salt diet (HSD)-induced Dahl salt-sensitive rats hypertensive renal injury led to decreased SIRT3 expression and an increase in EMT and oxidative stress. In contrast, Cana administration rescued SIRT3 expression, decreased both EMT and levels of oxidative stress, and ameliorated renal injury. Furthermore, we compared the antihypertensive and renoprotective properties of Cana when combined with irbesartan (Irb), a renin-angiotensin system (RAS) blocker. We concluded that administration of Cana in combination with Irb had a significantly greater effect in lowering systolic blood pressure when compared to Cana monotherapy. However, no statistical differences were observed between combined therapy and monotherapy groups with regards to the lowering of diastolic blood pressure and renoprotection. Utilizing the human renal proximal tubular epithelial cell line (HK-2), Angiotensin II (AngⅡ) induced HK-2 negatively regulated the expression of SIRT3, FOXO3a, catalase, and promoted EMT, all of which were reversed by Cana. Furthermore, SIRT3 silencing abolished Cana-mediated rescue of forkhead box O3a (FOXO3a) and catalase expression and Cana-mediated suppression of EMT in AngⅡ induced HK-2. Taken together, Cana acts as a renoprotective agent by suppressing EMT in the pathology of renal fibrosis via interaction with the SIRT3-FOXO3a pathway.

Supressed plasma renin in patients with primary hypertension is thought to be an indirect marker of sodium-induced volume expansion which is associated with more severe hypertension and hypertension-mediated organ damage. A novel test for erythrocyte glycocalyx sensitivity to sodium (eGCSS) has been proposed as a direct measure of sodium-induced damage on erythrocyte surfaces and a marker of sensitivity of the endothelium to salt in humans. Here we explore if eGCSS relates to plasma renin and other clinical and biochemical characteristics in a cohort of patients with primary hypertension. Hypertensive subjects (n = 85, 54% male) were characterised by blood biochemistry (including plasma renin/aldosterone), urine analysis for albumin-creatinine ratio (ACR), 24-h urine sodium/potassium excretion. eGCSS was measured using a commercially available kit. Correlations between eGCSS and clinical and biochemical characteristics were explored using Spearman's correlation coefficient and characteristics compared across tertiles of eGCSS. eGCSS was inversely correlated with renin (p < 0.05), with renin 17.72 ± 18 µU/l in the highest tertile of eGCSS compared to 84.27 ± 146.5 µU/l in the lowest (p = 0.012). eGCSS was positively correlated with ACR (p < 0.01), with ACR 7.37 ± 15.29 vs. 1.25 ± 1.52 g/mol for the highest vs. lowest tertiles of eGCSS (p < 0.05). eGCSS was not correlated with other clinical characteristics or biochemical measures. These results suggests that sodium retention in hypertension characterised by a low-renin state is associated with cell membrane damage reflected by eGCSS. This may contribute to the hypertension-mediated organ damage and the excess mortality associated with sodium overload and "salt sensitivity".

Primary aldosteronism (PA) is a frequent cause of hypertension. Aldosterone excess together with high dietary salt intake aggravates cardiovascular damage, despite guideline-recommended mineralocorticoid receptor antagonist (MRA) treatment.

To investigate the antihypertensive impact of a moderate dietary salt restriction and associated physiological changes, including mental well-being.

A total of 41 patients with PA on a stable antihypertensive regimen-including MRA-followed a dietary salt restriction for 12 weeks with structured nutritional training and consolidation by a mobile health app. Salt intake and adherence were monitored every 4 weeks using 24-h urinary sodium excretion and nutrition protocols. Body composition was assessed by bioimpedance analysis and mental well-being by validated questionnaires.

Dietary salt intake significantly decreased from 9.1 to 5.2 g/d at the end of the study. In parallel, systolic (130 vs. 121 mm Hg) and diastolic blood pressure (BP) (84 vs. 81 mm Hg) improved significantly. Patients' aptitude of estimating dietary salt content was refined significantly (underestimation by 2.4 vs. 1.4 g/d). Salt restriction entailed a significant weight loss of 1.4 kg, improvement in pulse pressure (46 vs. 40 mm Hg) and normalization of depressive symptoms (PHQD scale, p < 0.05). Salt restriction, cortisol after dexamethasone suppression test and dosage of renin-angiotensin-aldosterone-system (RAAS) blockers were independently associated with BP reduction.

A moderate restriction of dietary salt intake in patients with PA substantially reduces BP and depressive symptoms. Moreover, the findings underline that a sufficient RAAS blockade seems to augment the effects of salt restriction on BP and cardiovascular risk.

Hypertension is the most important modifiable risk factor for cardiovascular disease and a leading public health concern.

The primary aim was to compare sequential nephron blockade (SNB) versus dual renin-angiotensin system blockade (DRASB) plus bisoprolol in patients with resistant hypertension to observe reductions in systolic and diastolic blood pressure (SBP and DBP) levels after 20 weeks of treatment.

This trial was an open-label, prospective, randomized, parallel-group, clinical study with optional drug up-titration. Participants were evaluated during five visits at 28-day intervals.

The mean age was 55.5 years in the SNB and 58.4 years in the DRASB + bisoprolol group (p=NS). Significant office BP reductions were observed in both groups. SNB group, SBP decreased from 174.5±21.0 to 127.0±14.74 mmHg (p<0.0001), and DBP decreased from 105.3±15.5 to 78.11±9.28 mmHg (p<0.0001). DRASB group, SBP decreased from 178.4±21.08 to 134.4 ± 23.25 mmHg (p<0.0001) and DBP decreased from 102.7±11.07 to 77.33±13.75 mmHg (p<0.0001). Ambulatory blood pressure monitoring (ABPM) showed also significant SBP and DBP reductions in both groups (p<0.0001).

In patients with RHTN adherent to treatment, SNB and DRASB plus bisoprolol showed excellent therapeutic efficacy, although SNB was associated with earlier SBP reduction.

Hypertension is a significant public health problem that affects people all over the world. Various epidemiologic researches have been conducted to reveal the relationship between hypertension and several biochemical markers. The goal of this project was to investigate the electrolytes, glucose, total protein, and lipid profile in people with normal and high blood pressure.

Between 2020 and 2022, a case-control study was done. Two hundred and eighteen males, age ranging from 30 to 70, took part in the study. The conventional flame photometric method was used to evaluate serum electrolytes, whereas kits from Biolab Company's kits were used to quantify serum calcium, serum glucose, and lipid profile.

When compared to normotension males, hypertension males had considerably greater salt, chloride, and potassium levels in their blood, but no significant variations in calcium levels. When compared to normotension males, hypertension individuals had considerably higher mean glucose, total cholesterol, low, and high-density lipoprotein cholesterol, and triglycerides. Many amino acids were identified in the blood of male hypertension patients, consisting of leucine, aspartic acid, glutamic acid, asparagine, serine, histidine, glycine, arginine, alanine, methionine, valine, and phenylalanine.

In this group, hypertension males have a different lipid and electrolyte profile than normotensive males.

Orthostatic hypotension affects roughly 10% of individuals with hypertension and is associated with several adverse health outcomes, including dementia, cardiovascular disease, stroke, and death. Among adults with hypertension, orthostatic hypotension has also been shown to predict patterns of blood pressure dysregulation that may not be appreciated in the office setting, including nocturnal nondipping. Individuals with uncontrolled hypertension are at particular risk of orthostatic hypotension and may meet diagnostic criteria for the condition with a smaller relative reduction in blood pressure compared with normotensive individuals. Antihypertensive medications are commonly de-prescribed to address orthostatic hypotension; however, this approach may worsen supine or seated hypertension, which may be an important driver of adverse events in this population. There is significant variability between guidelines for the diagnosis of orthostatic hypotension with regards to timing and position of blood pressure measurements. Clinically relevant orthostatic hypotension may be missed when standing measurements are delayed or when taken after a seated rather than supine position. The treatment of orthostatic hypotension in patients with hypertension poses a significant management challenge for clinicians; however, recent evidence suggests that intensive blood pressure control may reduce the risk of orthostatic hypotension. A detailed characterization of blood pressure variability is essential to tailoring a treatment plan and can be accomplished using both in-office and out-of-office monitoring.

Isolated systolic hypertension is associated with higher risk of cardiovascular disease and all-cause mortality. Despite being the most common form of hypertension in the elderly, it is also detectable among young and middle-aged subjects. Dietary salt (sodium chloride) intake is an important determinant of blood pressure, and high salt intake is associated with greater risk of hypertension and cardiovascular events. In most countries, habitual salt intake at all age categories largely exceeds the international recommendations. Excess salt intake, often interacting with overweight and insulin resistance, may contribute to the development and maintenance of isolated systolic hypertension in young individuals by causing endothelial dysfunction and promoting arterial stiffness through a number of mechanisms, namely increase in the renin-angiotensin-aldosterone system activity, sympathetic tone and salt-sensitivity. This short review focused on the epidemiological and clinical evidence, the mechanistic pathways and the cluster of pathophysiological factors whereby excess salt intake may favor the development and maintenance of isolated systolic hypertension in young people.

Most hypertensive cases are primary and heavily associated with modifiable risk factors like salt intake. Evidence suggests that even small reductions in salt consumption reduce blood pressure in all age groups. In that regard, the ACC/AHA described a distinct set of individuals who exhibit salt-sensitivity, regardless of their hypertensive status. Data has shown that salt-sensitivity is an independent risk factor for cardiovascular events and mortality. However, despite extensive research, the pathogenesis of salt-sensitive hypertension is still unclear and tremendously challenged by its multifactorial etiology, complicated genetic influences, and the unavailability of a diagnostic tool. So far, the important roles of the renin-angiotensin-aldosterone system, sympathetic nervous system, and immune system in the pathogenesis of salt-sensitive hypertension have been studied. In the first part of this review, we focus on how the systems mentioned above are aberrantly regulated in salt-sensitive hypertension. We follow this with an emphasis on genetic variants in those systems that are associated with and/or increase predisposition to salt-sensitivity in humans.

To evaluate the interaction effect of blood glucose and blood pressure on the risk of chronic kidney disease (CKD).

31,165 subjects were selected without CKD at baseline and had completed the first follow-up from "Jinchang cohort". Cox regression model and restricted cubic splines functions were used to evaluate the effects of blood glucose or pressure on the incidence of CKD and dose-response relationship after adjusting for confounding covariates. Synergic effect was assessed by the multiplicative or additive interaction scale.

Among 31,165 subjects, 1307 new-onset CKD were observed during 68905.78 person-years follow-up, and the incidence density was 18.97 per 1000 person-years. The risk of CKD gradually increased with the increase of blood pressure in diabetes, pre-diabetes and normal groups (P_trend < 0.05). And, the risk was greatest when SBP/DBP reached ≥150/≥110 mmHg in three groups, and HRs (95% CI) were 1.610 (1.070-2.422), 2.142 (1.396-3.288) and 2.455 (1.941-3.106), respectively. Additionally, among hypertension, pre-hypertension and normal groups, the risk of CKD increased by 16.0%, 14.3% and 25.2% for each 1 mmol/L of FPG. When FPG level was more than 9.0 mmol/L, the risk was greatest and adjusted HRs (95% CI) were 2.856 (2.176-3.748), 2.979 (1.828-4.854) and 7.520 (4.517-12.519). Furthermore, the risk was highest when hypertension was accompanied by diabetes (HR = 4.915, 95% CI: 3.923-6.157). This analysis supported a less than multiplicative effect (HR = 0.634, 95% CI: 0.417-0.964) for the interaction term of diabetes and hypertension, while there was no additive interaction towards CKD in all interaction term.

Blood glucose and pressure were independent risk factors in incidence of CKD, but there was only a negative multiplicative interaction between hypertension and diabetes, but no additive interaction effect between them.

Tumor Necrosis Factor (TNF)-α is a proinflammatory cytokine (PIC) and has been implicated in a variety of illness including cardiovascular disease. The current study investigated the inflammatory response trigged by TNFα in both cultured brain neurons and the hypothalamic paraventricular nucleus (PVN), a key cardiovascular relevant brain area, of the Sprague Dawley (SD) rats. Our results demonstrated that TNFα treatment induces a dose- and time-dependent increase in mRNA expression of PICs including Interleukin (IL)-1β and Interleukin-6 (IL6); chemokines including C-C Motif Chemokine Ligand 5 (CCL5) and C-C Motif Chemokine Ligand 12 (CCL12), inducible nitric oxide synthase (iNOS), as well as transcription factor NF-kB in cultured brain neurons from neonatal SD rats. Consistent with this finding, immunostaining shows that TNFα treatment increases immunoreactivity of IL1β, CCL5, iNOS and stimulates activation or expression of NF-kB, in both cultured brain neurons and the PVN of adult SD rats. We further compared mRNA expression of the aforementioned genes in basal level as well as in response to TNFα challenge between SD rats and Dahl Salt-sensitive (Dahl-S) rats, an animal model of salt-sensitive hypertension. Dahl-S brain neurons presented higher baseline levels as well as greater response to TNFα challenge in mRNA expression of CCL5, iNOS and IL1β. Furthermore, central administration of TNFα caused significant higher response in CCL12 in the PVN of Dahl-S rats. The increased inflammatory response to TNFα in Dahl-S rats may be indicative of an underlying mechanism for enhanced pressor reactivity to salt intake in the Dahl-S rat model.

Equisetum arvense L. (EA) is a traditional phytomedicine used as a diuretic agent worldwide and regulated strictly by European Medicine Agency (EMA) and Brazilian National Health Surveillance Agency (ANVISA). However, few studies evaluating its efficacy and safety have been published and no clinical trial assessing its antihypertensive effect has been reported to date.

To assess antihypertensive effect, safety and tolerability of EA compared to hydrochlorothiazide (HCTZ).

This is a double-blind randomized clinical trial, allocating 58 systemic arterial hypertension (SAH) stage I patients (both sexes, 25-65 years old) into two groups (EA and HCTZ). All patients underwent biochemical and cardiologic checkup prior to and during interventions. The EA standardized dry extract (900 mg/day) or HCTZ (25 mg/day) were administered for 3 months and follow-up visits were conducted every 30 days. Efficacy established goals were systolic blood pressure (SBP) and/or diastolic blood pressure (DBP) decreases ≥ 10.0 mmHg and/or casual blood pressure (CBP) < 140/90 mmHg.

EA treatment demonstrated a significant antihypertensive effect, promoting a mean decrease of SBP and DBP by 12.6 and 8.1 mmHg, respectively, and resulting a CBP mean of 134.0/84.5 mmHg at the end of intervention on the SAH stage I patients (CBP mean of 148.5/95.7 mmHg). There were no significant statistical differences between EA and HCTZ interventions on blood pressure decrease, and before-after treatments regarding to biochemical tests and signs of acute toxicity, renal, hepatic and hematologic alterations. A slight trend but no significant difference were observed between adverse events from EA (3.58%) and HCTZ (4.68%) groups.

EA standardized dry extract was successfully applied to the SAH stage I patient treatment, decreasing effectively SBP ad DBP values to the reference normal ranges, and demonstrating a well-tolerability profile similar to HCTZ intervention.

The Himalayan salt (HS) has become a popular alternative for the traditional table salt (TS) due to its health benefit claims, particularly for individuals with arterial hypertension. However, despite the increase in HS consumption, there is still a lack of clinical evidence to support a recommendation for its consumption by health professionals.

This cross-over study aimed to compare the impact of HS and TS intake on systolic blood pressure (SBP) and diastolic blood pressure (DBP), and urinary sodium concentration in individuals with arterial hypertension.

This study recruited 17 female patients with arterial hypertension who ate out no more than once a week. Participants were randomized into two groups, to receive and consume either HS or TS. Before and after each intervention, participants had their blood pressure measured and urine collected for mineral analysis. A p-value < 0.05 was considered statistically significant.

There were no statistically significant differences before and after the HS intervention for DBP (70mmHg vs. 68.5mmHg; p=0.977), SBP (118.5 mmHg vs. 117.5 mmHg; p= 0.932) and sodium urinary concentration (151 mEq/24h vs. 159 mEq/24; p=0.875). Moreover, the between-group analysis showed no significant differences after the intervention regarding SBP (117mmHg vs 119 mmHg; p=0.908), DBP (68.5 mmHg vs. 71mmHg; p= 0,645) or sodium urinary concentration (159 mEq/24h vs. 155 mEq/24h; p=0.734).

This study suggests that there are no significant differences on the impact of HS consumption compared to TS on blood pressure and sodium urinary concentration in individuals with arterial hypertension.