The doses used were "For SHRs, the dosage of RESV was equivalent to ~ 146 mg RESV/kg/day and for mice, the dosage was equivalent to ~ 320 mg RESV/kg/day. "
SHR = spontaneously hypertensive rat
A lot of interesting effects noted in addition to reduced BP....
Biochim Biophys Acta. 2013 May 21. pii: S0925-4439(13)00180-4. doi: 10.1016/j.bbadis.2013.05.018. [Epub ahead of print]
Resveratrol Prevents Hypertension and Cardiac Hypertrophy in Hypertensive Rats and Mice.
Dolinsky VW, Chakrabarti S, Pereira TJ, Oka T, Levasseur J, Beker D, Zordoky BN, Morton JS, Nagendran J, Lopaschuk GD, Davidge ST, Dyck JR.
Source
Cardiovascular Research Centre, Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada; Manitoba Institute of Child Health, Department of Pharmacology and Therapeutics, University of Manitoba, Winnipeg, Manitoba, Canada.
Abstract
Resveratrol (RESV) is a polyphenol with pleiotropic effects that include reduction of oxidative stress and increased vascular nitric oxide (NO) production. However, whether or not RESV can prevent rises in blood pressure (BP) is controversial and remains to be firmly established. The purpose of this study was to determine whether RESV attenuates elevated BP and subsequent adaptive cardiac hypertrophy and to better understand the mechanisms involved. The spontaneously hypertensive rat (SHR) and the angiotensin (Ang)-II infused mouse were used as hypertensive models. Compared to a standard control diet, consumption of diets containing RESV by SHRs and Ang-II hypertensive mice, markedly prevented rises in systolic BP. In addition, flow-mediated vasodilation was significantly improved by RESV in SHRs. RESV also reduced serum and cardiac levels of the lipid peroxidation by-product, 4-hydroxy-2-nonenal in the hypertensive rodents and inhibited the production of superoxide in human-derived endothelial cells. Analysis of mesenteric arteries from SHRs and AngII-infused mice demonstrated that RESV increased endothelial NO synthase (eNOS) phosphorylation by enhancing the LKB1/AMP-activated protein kinase (AMPK) signal transduction pathway. Moreover, RESV reduced hypertrophic growth of the myocardium through reduced hemodynamic load and inhibition of the p70 S6 kinase pro-hypertrophic signalling cascade. Overall, we show that high dose RESV reduces oxidative stress, improves vascular function, attenuates high BP and prevents cardiac hypertrophy through the preservation of the LKB1-AMPK-eNOS signalling axis.
Copyright © 2013. Published by Elsevier B.V.
PMID: 23707558
Edited by maxwatt, 06 June 2013 - 01:01 AM.
