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Chronic alcohol-induced oxidative endothelial injury relates to angiotensin II levels in the rat.
Mol Cell Biochem. 2008 Jan; 307(1-2):51-8.MC

Abstract

The link between chronic alcohol consumption and cardiovascular injury including hypertension is well known. However, molecular mediators implicated with alcohol-induced elevation in blood pressure (BP) remain elusive. The aim of this study was to investigate the relationship of chronic ethanol-induced endothelial injury and elevation in BP with angiotensin II levels in rats. Male Fisher rats were divided into two groups of seven animals each and treated as follows: (1) Control (5% sucrose, orally) daily for 12 weeks and (2) ethanol (4 g kg(-1), orally) daily for 12 weeks. The BP (systolic, diastolic, and mean) was recorded every week. The animals were anesthetized with pentobarbital after 12 weeks; blood and thoracic aorta were isolated and analyzed for aortic reactivity response, angiotensin II levels, and oxidative endothelial injury. The results show that the systolic, diastolic, and mean BP were significantly elevated 12 weeks after ethanol ingestion. The increased BP was related to elevated angiotensin II levels in the plasma and aorta of alcohol treated group compared to control. The aortic NADPH oxidase activity, ratio of oxidized to reduced glutathione (GSSG/GSH) and lipid peroxidation significantly increased, whereas nitric oxide (NO), endothelial NO synthase (eNOS), and vascular endothelial growth factor (VEGF) protein expressions were depressed in alcohol group compared to control. The phenylephrine-mediated vasoconstriction response was not altered, while acetylcholine-mediated vasorelaxation response was depressed in the aorta of ethanol treated rats compared to control. It is concluded that chronic ethanol ingestion induces hypertension which is correlated with elevated tissue angiotensin II levels, activation of NADPH oxidase activity causing endothelial injury, depletion of endothelial NO generating system, and impaired vascular relaxation in rats.

Authors+Show Affiliations

Department of Physiology, Pharmacology and Toxicology, Ponce School of Medicine, Ponce, PR 00732, USA. kazimhusain@hotmail.comNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

17721810

Citation

Husain, Kazim, et al. "Chronic Alcohol-induced Oxidative Endothelial Injury Relates to Angiotensin II Levels in the Rat." Molecular and Cellular Biochemistry, vol. 307, no. 1-2, 2008, pp. 51-8.
Husain K, Vazquez M, Ansari RA, et al. Chronic alcohol-induced oxidative endothelial injury relates to angiotensin II levels in the rat. Mol Cell Biochem. 2008;307(1-2):51-8.
Husain, K., Vazquez, M., Ansari, R. A., Malafa, M. P., & Lalla, J. (2008). Chronic alcohol-induced oxidative endothelial injury relates to angiotensin II levels in the rat. Molecular and Cellular Biochemistry, 307(1-2), 51-8.
Husain K, et al. Chronic Alcohol-induced Oxidative Endothelial Injury Relates to Angiotensin II Levels in the Rat. Mol Cell Biochem. 2008;307(1-2):51-8. PubMed PMID: 17721810.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Chronic alcohol-induced oxidative endothelial injury relates to angiotensin II levels in the rat. AU - Husain,Kazim, AU - Vazquez,Manuel, AU - Ansari,Rais A, AU - Malafa,Mokenge P, AU - Lalla,Jainarine, Y1 - 2007/08/25/ PY - 2007/05/03/received PY - 2007/08/10/accepted PY - 2007/8/28/pubmed PY - 2008/4/11/medline PY - 2007/8/28/entrez SP - 51 EP - 8 JF - Molecular and cellular biochemistry JO - Mol Cell Biochem VL - 307 IS - 1-2 N2 - The link between chronic alcohol consumption and cardiovascular injury including hypertension is well known. However, molecular mediators implicated with alcohol-induced elevation in blood pressure (BP) remain elusive. The aim of this study was to investigate the relationship of chronic ethanol-induced endothelial injury and elevation in BP with angiotensin II levels in rats. Male Fisher rats were divided into two groups of seven animals each and treated as follows: (1) Control (5% sucrose, orally) daily for 12 weeks and (2) ethanol (4 g kg(-1), orally) daily for 12 weeks. The BP (systolic, diastolic, and mean) was recorded every week. The animals were anesthetized with pentobarbital after 12 weeks; blood and thoracic aorta were isolated and analyzed for aortic reactivity response, angiotensin II levels, and oxidative endothelial injury. The results show that the systolic, diastolic, and mean BP were significantly elevated 12 weeks after ethanol ingestion. The increased BP was related to elevated angiotensin II levels in the plasma and aorta of alcohol treated group compared to control. The aortic NADPH oxidase activity, ratio of oxidized to reduced glutathione (GSSG/GSH) and lipid peroxidation significantly increased, whereas nitric oxide (NO), endothelial NO synthase (eNOS), and vascular endothelial growth factor (VEGF) protein expressions were depressed in alcohol group compared to control. The phenylephrine-mediated vasoconstriction response was not altered, while acetylcholine-mediated vasorelaxation response was depressed in the aorta of ethanol treated rats compared to control. It is concluded that chronic ethanol ingestion induces hypertension which is correlated with elevated tissue angiotensin II levels, activation of NADPH oxidase activity causing endothelial injury, depletion of endothelial NO generating system, and impaired vascular relaxation in rats. SN - 0300-8177 UR - https://www.unboundmedicine.com/medline/citation/17721810/Chronic_alcohol_induced_oxidative_endothelial_injury_relates_to_angiotensin_II_levels_in_the_rat_ DB - PRIME DP - Unbound Medicine ER -