Self-myofascial release (SMR) is a form of self-massage aiming to release tension, improve blood flow, and alleviate muscle soreness. This study aimed to determine whether a single session of SMR could impact cardiovascular parameters at rest and during a cold pressor test (CPT).

Twenty male participants (aged 26 ± 2 years) underwent a 20-min SMR and a 20-min seated control condition (CON) on two separate test days in a randomized order. Peripheral and central blood pressure (BP), total peripheral resistance (TPR), pulse wave velocity (PWV), heart rate (HR), root mean square of successive RR interval differences (RMSSD), and the quotient of low-frequency power and high-frequency power (LF/HF) were measured both at rest and during a CPT before (t0), 2 min (t1), and 20 min (t2) after the SMR and CON.

Time × condition interactions could be detected for peripheral and central diastolic BP, TPR, HR, and RMSSD. Following the SMR, peripheral diastolic BP, central diastolic BP, TPR, and RMSSD were reduced, while HR was increased compared to the CON. Regarding the CPT time × condition interactions could be detected for peripheral, and central diastolic BP, with lower values after SMR.

The results of the present study suggest that a single bout of SMR confers favorable cardiovascular benefits in healthy normotensive individuals. Furthermore, SMR can attenuate the hemodynamic reactivity to a stress test. Future research should address whether regular SMR leads to chronic adaptations similar to regular, moderate aerobic exercise, massage therapy, and static stretching.

Essential hypertension involves complex cardiovascular regulation. The autonomic nervous system function fluctuates throughout the sleep-wake cycle and changes with advancing age. However, the precise role of the autonomic nervous system in the development of hypertension during aging remains unclear. In this study, we characterized autonomic function during the sleep-wake cycle in different age groups with essential hypertension. This study included 97 men (53 with and 44 without hypertension) aged 30-79 years. They were stratified by age into young (< 40 years), middle-aged (40-59 years), and older (60-79 years) groups. Polysomnography and blood pressure data were recorded for 2 min before and during an hour-long nap. Autonomic function was assessed by measuring heart rate variability and blood pressure variability. Data were analyzed using t tests, correlation analyses, and two-way analysis of variance. During nonrapid eye movement (nREM), a main effect of age was observed on cardiac parasympathetic measures and baroreflex sensitivity (BRS), with the highest and lowest levels noted in the younger and older groups, respectively. The coefficients of the correlations between these measures and age were lower in patients with hypertension than in normotensive controls. The BRS of young patients with hypertension was similar to that of their middle-aged and older counterparts. However, cardiac sympathetic activity was significantly higher (p = 0.023) and BRS was significantly lower (p = 0.022) in the hypertension group than in the control group. During wakefulness, the results were similar although some of the above findings were absent. Autonomic imbalance, particularly impaired baroreflex, plays a more significant role in younger patients with hypertension. The nREM stage may be suitable for gaining insights into the relevant mechanisms.

The incidence of hypertension with diabetes mellitus (DM) as a co-morbid condition is on the rise worldwide. In 2000, an estimated 972 million adults had hypertension, which is predicted to grow to 1.56 billion by 2025. Hypertension often leads to diabetes mellitus that strongly puts the patients at an increased risk of cardiovascular, kidney, and/or atherosclerotic diseases. Hypertension has been identified as a major risk factor for the development of diabetes; patients with hypertension are at two-to-three-fold higher risk of developing diabetes than patients with normal blood pressure (BP). Causes for the increase in hypertension and diabetes are not well understood, environmental factors (e.g., exposure to environmental toxicants like heavy metals, organic solvents, pesticides, alcohol, and urban lifestyle) have been postulated as one of the reasons contributing to hypertension and cardiovascular diseases (CVD). The mechanism of action(s) of these toxicants in developing hypertension and CVDs is not well defined. Research studies have linked hypertension with the chronic consumption of alcohol and exposure to metals like lead, mercury, and arsenic have also been linked to hypertension and CVD. Workers chronically exposed to styrene have a higher incidence of CVD. Recent studies have demonstrated that exposure to particulate matter (PM) in diesel exhaust and urban air contributes to increased CVD and mortality. In this review, we have imparted the role of environmental toxicants such as heavy metals, organic pollutants, PM, alcohol, and some drugs in hypertension and CVD along with possible mechanisms and limitations in extrapolating animal data to humans.

Leptomeningeal anastomoses (LMAs) are pial collaterals that perfuse the penumbra and important for stroke outcome. We previously showed LMAs from SHRs (spontaneously hypertensive rats) were vasoconstricted compared with normotensive Wistar rats. Here, we investigated mechanisms by which hypertension causes LMA vasoconstriction. SHRs were treated with the ACE (angiotensin-converting enzyme) inhibitor captopril, an Ang II (angiotensin II)-independent antihypertensive agent hydralazine, or vehicle for 5 weeks in drinking water (n=8/group). A group of Wistar rats (n=8) had regular drinking water served as controls. Blood pressure was measured twice weekly by tail-cuff. LMAs were isolated and studied under pressurized conditions. Vasoreactivity of LMAs, including myogenic responses, reactivity to Rho-kinase inhibitor Y-27632, and nitric oxide were measured. Both captopril and hydralazine lowered blood pressure in SHRs similar to Wistar. However, only captopril normalized LMA increased tone compared with untreated SHRs (15±2% versus 50±3%; P<0.01) that was similar to Wistar (16±2%) but not hydralazine (38±6%; P>0.05). Vasodilatory response of LMAs to Y-27632 was impaired in SHRs compared with Wistar (28±3% versus 81±4%; P<0.01) that was restored by captopril (84±5%; P<0.01) and partially hydralazine (59±4%). LMAs from all groups constricted similarly to NOS (NO synthase) inhibition; however, the vasodilatory response of LMAs to the nitric oxide donor sodium nitroprusside was impaired in SHRs compared with Wistar rats (29±4% versus 80±2%; P<0.01) that was restored by captopril (84±4%; P<0.01), not hydralazine (38±8%; P>0.05). These results suggest that ACE inhibition during chronic hypertension reversed vascular dysfunction and hyperconstriction of LMAs that could improve stroke outcome by increasing collateral perfusion.

Homeostasis is a founding principle of integrative physiology. In current systems biology, however, homeostasis seems almost invisible. Is homeostasis a key goal driving body processes, or is it an emergent mechanistic fact? In this perspective piece, I propose that the integrative physiological and systems biological viewpoints about homeostasis reflect different epistemologies, different philosophies of knowledge. Integrative physiology is concept driven. It attempts to explain biological phenomena by continuous formation of theories that experimentation or observation can test. In integrative physiology, "function" refers to goals or purposes. Systems biology is data driven. It explains biological phenomena in terms of "omics"-i.e., genomics, gene expression, epigenomics, proteomics, and metabolomics-it depicts the data in computer models of complex cascades or networks, and it makes predictions from the models. In systems biology, "function" refers more to mechanisms than to goals. The integrative physiologist emphasizes homeostasis of internal variables such as Pco₂ and blood pressure. The systems biologist views these emphases as teleological and unparsimonious in that the "regulated variable" (e.g., arterial Pco₂ and blood pressure) and the "regulator" (e.g., the "carbistat" and "barostat") are unobservable constructs. The integrative physiologist views systems biological explanations as not really explanations but descriptions that cannot account for phenomena we humans believe exist, although they cannot be observed directly, such as feelings and, ultimately, the conscious mind. This essay reviews the history of the two epistemologies, emphasizing autonomic neuroscience. I predict rapprochement of integrative physiology with systems biology. The resolution will avoid teleological purposiveness, transcend pure mechanism, and incorporate adaptiveness in evolution, i.e., "Darwinian medicine."

Taurine is an abundant, free amino acid found in mammalian cells that contributes to many physiologic functions from that of a simple cell osmolyte to a programmer of adult health and disease. Taurine's contribution extends from conception throughout life, but its most critical exposure period is during perinatal life. In adults, taurine supplementation prevents or alleviates cardiovascular disease and related complications. In contrast, low taurine consumption coincides with increased risk of cardiovascular disease, obesity and type II diabetes. This review focuses on the effects that altered perinatal taurine exposure has on long-term mechanisms that control adult arterial blood pressure and could thereby contribute to arterial hypertension through its ability to program these cardiovascular regulatory mechanisms very early in life. The modifications of these mechanisms can last a lifetime and transfer to the next generation, suggesting that epigenetic mechanisms underlie the changes. The ability of perinatal taurine exposure to influence arterial pressure control mechanisms and hypertension in adult life appears to involve the regulation of growth and development, the central and autonomic nervous system, the renin-angiotensin system, glucose-insulin interaction and changes to heart, blood vessels and kidney function.

Generation of angiotensin II (Ang II) contributes to the pathogenesis of cardiovascular diseases. Owing to the existence of high levels of Ang II within the kidney, blockade of the intrarenal Ang II levels may be important since long term outcome seems not only to be related to blood pressure per se. This was a prospective, randomized, double-blind, placebo-controlled study, with crossover design. We examined in 13 patients with mild to moderate hypertension the specific systemic and renal blocking properties of two different Ang II receptor blockers during a wide range of Ang II concentrations, 24 h post dose. The effects were evaluated after 4 weeks treatment with candesartan cilexetil (16 mg OD), losartan (50 mg OD) and placebo using clearance techniques. Candesartan reduced the 24 h blood pressure better than losartan (138(*)/87+/-12/8 vs 145/89+/-12/7 mmHg, (*)P<0.05 vs losartan) and placebo. Despite the lower blood pressure, candesartan attenuated the Ang II-induced response on ERPF and RVR markedly better than losartan or placebo. The GFR decreased, as expected, with placebo, but remained stable with candesartan. The present study demonstrates that in hypertensive patients candesartan and to a lesser degree losartan are effective in blocking the systemic and renal effects of Ang II during a wide range of Ang II infusion rates. Interestingly, 24 h post dose, candesartan effectively diminished the change in ERPF as well as GFR. This sustained renal effect of candesartan may be of importance, especially in pathophysiological circumstances in which (high renal levels of) Ang II contributes to cardiovascular damage.

Hypertension is a very frequent disease, known to trigger a range of severe cardiovascular problems. The elucidation of its pathophysiology requires investigation of the mechanisms responsible for the maintenance of blood pressure in the normal system, and their possible failure in hypertension. Some of these control mechanisms display nonlinear features, indicating that the blood pressure signal might be characterized by nonlinear dynamics. Our aim was thus to investigate the nonlinear properties of the blood pressure signal under normal conditions, and in a cardiovascular system prone to hypertension. Blood pressure was investigated in young spontaneously hypertensive rats (SHR), versus their age-matched normotensive progenitors (WKY). The correlation dimension was computed as quantification of blood pressure control complexity. The parameters required for the calculation procedure of the correlation dimension were carefully determined. The results were tested with surrogate data statistics. assuming linear autocorrelated Gaussian noise as the null hypothesis. Non-integer correlation dimension values were found in both strains, with lower values for SHR than for WKY, in particular following alpha-blockade. In all cases, a statistically significant difference was found between the real and surrogate data. These results show that the nonlinear dynamics parameter D, can be used to detect differences in BP control between prehypertensive SHR and WKY rats as early as 6-7 weeks after birth.

This randomized, double-blind, placebo-controlled crossover study evaluated the effects of the angiotensin II type 1 (AT1)-receptor blocker candesartan cilexetil on renal blood perfusion and glomerular filtration in patients with primary hypertension with diastolic blood pressure of 100 to 114 mm Hg. After a 4-week placebo run-in period, patients were randomized to receive either 16 mg candesartan cilexetil or placebo once daily for 6 weeks, after which they were switched to the alternative treatment. At the end of each period, 24 h after the last dose, renal assessments were made and the plasma renin activity, plasma concentrations of angiotensin II, aldosterone, and catecholamines were measured. Compared with placebo, candesartan cilexetil significantly reduced mean arterial pressure, by 8 mm Hg (95% confidence interval [CI], 3;12). Renal vascular resistance was significantly reduced by 0.03 mm Hg/mL min(-1) (95% CI, 0.01; 0.06). There was a small nonsignificant increase in renal plasma flow. The filtration fraction fell slightly from 0.24 to 0.22 (95% CI, -0.00, 0.04). As expected, angiotensin II concentrations and plasma renin activity were increased and the aldosterone concentrations were reduced. Catecholamine concentrations were unaffected. In conclusion, 6 weeks' treatment with 16 mg candesartan cilexetil once daily induced a reduction of renal vascular resistance and a trend toward increased renal plasma flow despite a reduction in mean arterial pressure. Because the glomerular filtration rate was maintained the filtration fraction was reduced, indicating a decreased glomerular capillary pressure.

Insulin resistance may cause a metabolic syndrome but whether insulin resistance causes hypertension is very controversial. Furthermore, it remains unclear whether the link between the insulin-resistance-related metabolic syndrome and hypertension is different between men and women. We examined fasting insulin, glucose, triglyceride and high-density lipoprotein (HDL)-cholesterol levels, systolic blood pressure, body mass index, and waist-to-hip ratio in a dataset from 8437 nondiabetic residents (age range, 30 to 89 years) in Kinmen. Factor analysis, a multivariate correlation statistical technique, was used to investigate the clustering and interdependence of these risk variables. Factor analysis identified two factors for men (n = 3659) and three factors for women (n = 4778, respectively. In men, a cluster of insulin, triglyceride, HDL-cholesterol, body mass index, and waist-to-hip ratio (metabolic syndrome) accounted for 29.7%, and a cluster of systolic blood pressure and glucose (hyperglycemia plus hypertension) accounted for 18.1% of the total variance in all variables considered. In women, a cluster of insulin, triglyceride, body mass index, waist-to-hip ratio, and systolic blood pressure (metabolic syndrome plus hypertension) accounted for 29.4%, a cluster of systolic blood pressure, glucose, and triglyceride (hyperglycemia plus hypertension plus dyslipidemia) accounted for 14.0%, and a cluster of triglyceride and HDL-cholesterol (dyslipidemia) accounted for 16.2% of the total variance. In conclusion, a distinct insulin-resistance-related metabolic syndrome characterized by hyperinsulinemia, dyslipidemia, and obesity was observed for both men and women in this Chinese population. However, hypertension was linked to the metabolic syndrome in women only.

Stereospecific synthesis of cis and trans 3-substituted vinyl-gamma-aminobutyric acid analogs were obtained by either a Claisen rearrangement or a Wittig reaction from common diene precursors.

This research uses the diastolic decay constant (tau) to investigate the short term mechanism responsible for vasomotor control, mainly the alpha-sympathetic control system. Previous studies have shown that vasomotor control is altered in spontaneously hypertensive rats (SHR) preceding the phase of overt hypertension. The diastolic decay, according to the two element Windkessel model, displays an exponential shape with a decay constant, tau, depending on both the vascular resistance and the compliance. In our experiments, we used tau to characterize vasomotor activity and its control in the normotensive rats as well as in the spontaneously hypertensive rats (SHR) prone to hypertension. The beat to beat value of tau was evaluated from a continuous arterial blood pressure (ABP) signal, measured in the tail artery of the conscious, unrestrained rat. Four months old prehypertensive SHR were compared to their age matched normotensive controls (WKY). To study vasomotor regulation, we computed gains and delay times by investigating the compensatory response in tau to changes in mean ABP (MBP). These parameters are expected in the short term to be neurally controlled by the sympathetic system, mainly alpha-sympathetic. Our set of experiments consisted of changing MBP by performing successive injections in bolus of increasing doses of the vasoconstrictor angiotensin II. This procedure was repeated under double cardiac autonomic blockade of the vagal and beta 1 = sympathetic limbs. Our results show that, under baseline conditions, the absolute gain and delay times of tau are reduced in SHR compared to WKY. Double cardiac blockade decreases the absolute gain in both strains, while abolishing the baseline strain differences. These results reinforce our assumption that, in SHR, the alpha-sympathetic system is in a basic state of excitation even prior to the onset of overt hypertension and therefore reacting with reduced sensitivity (lower gain) to changes in MBP.