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Adiponectin opposes endothelin-1-mediated vasoconstriction in the perfused rat hindlimb

Citation

Bussey, CT and Kolka, CM and Rattigan, S and Richards, SM, Adiponectin opposes endothelin-1-mediated vasoconstriction in the perfused rat hindlimb, American Journal of Physiology: Heart and Circulatory Physiology, 301, (1) pp. H79-H86. ISSN 0363-6135 (2011) [Refereed Article]


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Copyright Statement

Copyright © 2011 the American Physiological Society

Official URL: http://www.the-aps.org/publications/authorinfo/cop...

DOI: doi:10.1152/ajpheart.00864.2010

Abstract

Recent studies have shown that adiponectin is able to increase nitric oxide (NO) production by the endothelium and relax preconstricted isolated aortic rings, suggesting that adiponectin may act as a vasodilator. Endothelin-1 (ET-1) is a potent vasoconstrictor, elevated levels of which are associated with obesity, type 2 diabetes, hypertension, and cardiovascular disease. We hypothesized that adiponectin has NO-dependent vascular actions opposing the vasoconstrictor actions of ET-1. We studied the vascular and metabolic effects of a physiological concentration of adiponectin (6.5 μg/ml) on hooded Wistar rats in the constant-flow pump-perfused rat hindlimb. Adiponectin alone had no observable vascular activity; however, adiponectin pretreatment and coinfusion inhibited the increase in perfusion pressure and associated metabolic stimulation caused by low-dose (1 nM) ET-1. Adiponectin was not able to oppose vasoconstriction when infusion was commenced after ET-1. This is in contrast to the NO donor sodium nitroprusside, which significantly reduced the pressure due to established ET-1 vasoconstriction, suggesting dissociation of the actions of adiponectin and NO. In addition, adiponectin had no effect on vasoconstriction caused by either high-dose (20 nM) ET-1 or low-dose (50 nM) norepinephrine. Our findings suggest that adiponectin has specific, apparently NO-independent, vascular activity to oppose the vasoconstrictor effects of ET-1. The hemodynamic actions of adiponectin may be an important aspect of its insulin-sensitizing ability by regulating access of insulin and glucose to myocytes. Imbalance in the relationship between adiponectin and ET-1 in obesity may contribute to the development of insulin resistance and cardiovascular disease.

Item Details

Item Type:Refereed Article
Keywords:skeletal muscle; vasculature; vasodilation; glucose metabolism
Research Division:Medical and Health Sciences
Research Group:Cardiorespiratory Medicine and Haematology
Research Field:Cardiology (incl. Cardiovascular Diseases)
Objective Division:Health
Objective Group:Clinical Health (Organs, Diseases and Abnormal Conditions)
Objective Field:Diabetes
Author:Bussey, CT (Miss Carol Bussey)
Author:Kolka, CM (Miss Cathryn Kolka)
Author:Rattigan, S (Professor Stephen Rattigan)
Author:Richards, SM (Dr Stephen Richards)
ID Code:71463
Year Published:2011
Web of Science® Times Cited:17
Deposited By:Menzies Institute for Medical Research
Deposited On:2011-07-19
Last Modified:2017-11-06
Downloads:0

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