Quercetin-Supplemented Diets Lower Blood Pressure and Attenuate Cardiac Hypertrophy in Rats With Aortic Constriction

Jalili, Thunder PhD*; Carlstrom, Justin PhD*; Kim, Sun BS*; Freeman, David PhD; Jin, Huifeng BS*; Wu, Tzu-Ching MS*; Litwin, Sheldon E. MD; David Symons, J. PhD*

Journal of Cardiovascular Pharmacology:
doi: 10.1097/01.fjc.0000211746.78454.50
Original Articles
Abstract

Quercetin (Q), a flavonoid found in berries and onions, can reduce blood pressure in hypertensive animals and inhibit signal transduction pathways in vitro that regulate cardiac hypertrophy. We hypothesized that quercetin could prevent cardiovascular complications in rats with abdominal aortic constriction (AAC). Rats consumed standard or Q-supplemented chow (1.5 g Q/kg chow) for 7 days before AAC or sham surgery (SHAM, n=15; AAC, n=15; SHAMQ, n=15; AACQ, n=14). Fourteen days after surgery, plasma and liver Q concentrations were elevated (P<0.05) and hepatic lipid oxidation was reduced (P<0.05) in Q-treated versus untreated rats. Carotid arterial blood pressure and cardiac hypertrophy were attenuated (P<0.05), and cardiac protein kinase C βII translocation was normalized (P<0.05) in AACQ versus AAC. Expression of cardiac β-myosin heavy-chain mRNA was also reduced in AACQ versus AAC (P<0.05). However, extracellular regulated kinase 1/2 phosphorylation was similar in AAC versus AACQ. The level of aortic endothelial dysfunction (wire myography) was also similar between AAC and AACQ, in spite of reduced aortic thickening in AACQ. Importantly, Q-treated rats did not show any deleterious changes in myocardial function (echocardiography). Our data supports an antihypertensive and antihypertrophic effect of Q in vivo in the absence of changes concerning vascular and myocardial function.

Author Information

*College of Health

School of Medicine, University of Utah, Salt Lake City, Utah

Department of Medicine, University of Western Ontario, London, ON, Canada N6A 5A5

Drs. Jalili and Carlstrom contributed equally to this study.

This study was funded in part by the Morrison Trust Foundation and University of Utah Research Council to T. J. and an American Heart Association National Affiliate Scientist Development Grant (0130099N) to J. D. S., and by funds provided by the University of Utah College of Health.

Reprints: Thunder Jalili, PhD, Division of Nutrition, 250 S. 1850 E, ♯214, Salt Lake City, UT 84112 (e-mail: thunder.jalili@m.cc.utah.edu).

Received for publication September 23, 2005; accepted March 13, 2006

© 2006 Lippincott Williams & Wilkins, Inc.