Kimura DC, Nagaoka MR, Borges DR, Kouyoumdjian M. Angiotensin II or epinephrine hemodynamic and metabolic responses in the liver of L-NAME induced hypertension and spontaneous hypertensive rats. World J Hepatol 2017; 9(17): 781-790 [PMID: 28660012 DOI: 10.4254/wjh.v9.i17.781]
Corresponding Author of This Article
Maria Kouyoumdjian, PhD, Associate Professor of Biochemistry, Department of Biochemistry, Federal University of São Paulo, Experimental Hepatology Laboratory, Rua Botucatu 862 (Edifício José Leal Prado), São Paulo 04023-900, Brazil. mariak.bioq@epm.br
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Basic Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
Share the Article
Kimura DC, Nagaoka MR, Borges DR, Kouyoumdjian M. Angiotensin II or epinephrine hemodynamic and metabolic responses in the liver of L-NAME induced hypertension and spontaneous hypertensive rats. World J Hepatol 2017; 9(17): 781-790 [PMID: 28660012 DOI: 10.4254/wjh.v9.i17.781]
World J Hepatol. Jun 18, 2017; 9(17): 781-790 Published online Jun 18, 2017. doi: 10.4254/wjh.v9.i17.781
Angiotensin II or epinephrine hemodynamic and metabolic responses in the liver of L-NAME induced hypertension and spontaneous hypertensive rats
Debora Conte Kimura, Marcia Regina Nagaoka, Durval Rosa Borges, Maria Kouyoumdjian
Debora Conte Kimura, Maria Kouyoumdjian, Department of Biochemistry, Federal University of São Paulo, Experimental Hepatology Laboratory, São Paulo 04023-900, Brazil
Marcia Regina Nagaoka, Department of Biosciences, Federal University of São Paulo, Experimental Hepatology Laboratory, Santos 11015-020, Brazil
Durval Rosa Borges, Department of Medicine, Federal University of Sao Paulo, Experimental Hepatology Laboratory, São Paulo 04023-900, Brazil
Author contributions: Kimura DC contributed to the study in the areas of data acquisition, analysis, and interpretation, as well as revision and final approval of the paper; Borges DR made substantial contributions to the study; Nagaoka MR and Kouyoumdjian M contributed to study conception and design, analysis and interpretation, and paper preparation, revision, and final approval; all authors read and approved the final manuscript.
Supported byFundação de Amparo à Pesquisa do Estado de São Paulo, No. FAPESP, 2011/13974-8; and Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES).
Institutional review board statement: Approved by the Ethics in Research Committee of UNIFESP.
Institutional animal care and use committee statement: All procedures involving animals were reviewed and approved by the Ethics in Research Committee of UNIFESP, protocol number: (CEP 1455/09).
Conflict-of-interest statement: To the best of our knowledge, no conflict of interest exists.
Data sharing statement: No additional data are avaiable.
Correspondence to: Maria Kouyoumdjian, PhD, Associate Professor of Biochemistry, Department of Biochemistry, Federal University of São Paulo, Experimental Hepatology Laboratory, Rua Botucatu 862 (Edifício José Leal Prado), São Paulo 04023-900, Brazil. mariak.bioq@epm.br
Telephone: +55-11-55764502-2128
Received: December 15, 2016 Peer-review started: December 19, 2016 First decision: March 28, 2017 Revised: April 28, 2017 Accepted: May 18, 2017 Article in press: May 19, 2017 Published online: June 18, 2017 Processing time: 181 Days and 2.7 Hours
Abstract
AIM
To study hepatic vasoconstriction and glucose release induced by angiotensin (Ang)II or Epi in rats with pharmacological hypertension and spontaneously hypertensive rat (SHR).
METHODS
Isolated liver perfusion was performed following portal vein and vena cava cannulation; AngII or epinephrine (Epi) was injected in bolus and portal pressure monitored; glucose release was measured in perfusate aliquots.
RESULTS
The portal hypertensive response (PHR) and the glucose release induced by AngII of L-NAME were similar to normal rats (WIS). On the other hand, the PHR induced by Epi in L-NAME was higher whereas the glucose release was lower compared to WIS. Despite the similar glycogen content, glucose release induced by AngII was lower in SHR compared to Wistar-Kyoto rats although both PHR and glucose release induced by Epi in were similar.
CONCLUSION
AngII and Epi responses are altered in different ways in these hypertension models. Our results suggest that inhibition of NO production seems to be involved in the hepatic effects induced by Epi but not by AngII; the diminished glucose release induced by AngII in SHR is not related to glycogen content.
Core tip: Angiotensin (Ang)II and epinephrine (Epi) induce hemodynamic and metabolic responses in a normal liver. These responses are altered in different ways in two models of hypertension. We observed that inhibition of NO production seems to be involved in the hepatic hemodynamic and metabolic effects induced by Epi but not by AngII. Furthermore, diminished glucose release induced by AngII in spontaneously hypertensive rat is not related to glycogen content, but might be due to the glycogen phosphorylase activation by AngII.
