Document Detail


Calorie restriction prevents hypertension and cardiac hypertrophy in the spontaneously hypertensive rat.
MedLine Citation:
PMID:  20696994     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Because recent evidence demonstrated that calorie restriction (CR) has numerous beneficial cardiovascular effects, we investigated whether short-term CR could reduce hypertension and prevent cardiac hypertrophy inherent to the nonobese spontaneously hypertensive rat (SHR). After 5 weeks of either ad libitum feeding or short-term CR, SHRs subjected to short-term CR had lower systolic blood pressure (BP) and reduced left ventricular wall thickness as assessed by noninvasive tail-cuff BP measurements and echocardiography, respectively. In addition, ultrasound measurements of the femoral artery revealed that flow-mediated vasodilation was significantly improved in SHRs with CR compared to controls. Moreover, pressure myography of isolated mesenteric arteries and subsequent histological and biochemical analysis of these arteries demonstrated that short-term CR improved vascular compliance, increased endothelial nitric oxide synthase (eNOS) activity and nitric oxide bioavailability, and reduced vascular remodeling compared to ad libitum-fed SHRs. Although these effects are likely multifactorial, they were associated with elevated levels of the circulating adipokine, adiponectin, and enhanced AMP-activated protein kinase (AMPK) activity. To provide evidence that elevated adiponectin levels in the SHR is sufficient to prevent an increase in BP, adenoviral-mediated overexpression of adiponectin increased circulating levels of adiponectin, reduced BP, and activated the AMPK/eNOS pathway in the absence of CR. Overall, our findings provide compelling evidence that short-term CR exerts beneficial effects in the SHR via stimulation of an adiponectin/AMPK/eNOS signaling axis. As a result, CR may serve as an effective nonpharmacological treatment of hypertension, and targeting the adiponectin/AMPK/eNOS pathway may improve treatment of hypertension.
Authors:
Vernon W Dolinsky; Jude S Morton; Tatsujiro Oka; Isabelle Robillard-Frayne; Mariel Bagdan; Gary D Lopaschuk; Christine Des Rosiers; Kenneth Walsh; Sandra T Davidge; Jason R B Dyck
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-08-09
Journal Detail:
Title:  Hypertension     Volume:  56     ISSN:  1524-4563     ISO Abbreviation:  Hypertension     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-08-19     Completed Date:  2010-09-13     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  United States    
Other Details:
Languages:  eng     Pagination:  412-21     Citation Subset:  IM    
Affiliation:
458 Heritage Medical Research Centre, University of Alberta, Edmonton, Alberta T6G 2S2, Canada. jason.dyck@ualberta.ca
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MeSH Terms
Descriptor/Qualifier:
AMP-Activated Protein Kinases / metabolism
Adipokines / blood
Animals
Blood Pressure / physiology
Caloric Restriction*
Cardiomegaly / prevention & control*
Femoral Artery / physiology
Hypertension / metabolism,  prevention & control*
Rats
Rats, Inbred SHR
Regional Blood Flow / physiology
Statistics, Nonparametric
Grant Support
ID/Acronym/Agency:
//Canadian Institutes of Health Research
Chemical
Reg. No./Substance:
0/Adipokines; EC 2.7.11.1/AMP-Activated Protein Kinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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