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


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 © 2011 the American Physiological Society

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DOI: doi:10.1152/ajpheart.00864.2010


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:Biomedical and Clinical Sciences
Research Group:Cardiovascular medicine and haematology
Research Field:Cardiology (incl. cardiovascular diseases)
Objective Division:Health
Objective Group:Clinical health
Objective Field:Clinical health not elsewhere classified
UTAS Author:Bussey, CT (Miss Carol Bussey)
UTAS Author:Kolka, CM (Miss Cathryn Kolka)
UTAS Author:Rattigan, S (Professor Stephen Rattigan)
UTAS Author:Richards, SM (Dr Stephen Richards)
ID Code:71463
Year Published:2011
Web of Science® Times Cited:21
Deposited By:Menzies Institute for Medical Research
Deposited On:2011-07-19
Last Modified:2017-11-06

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