Contribution of NO, ATP-sensitive K+ channels and prostaglandins to adenosine receptor agonists-induced relaxation of the rat tail artery.
Journal Title: Pharmacological Reports - Year 2009, Vol 61, Issue 2
Abstract
The mechanism of relaxation in the rat tail artery induced by the adenosine A(1) receptor-selective agonist N(6)-cyclohexyladenosine (CHA, 10 nM-300 microM) and the adenosine A1/A(2a) receptor agonist 5'-N-ethylcarboxamidoadenosine (NECA, 10 nM-300 microM) has been characterized. To do this, we used alpha(1)-receptor agonist phenylephrine to evoke contraction (10 microM), and inhibitors of nitric oxide synthase (L-NAME, 10 microM), ATP-sensitive K(+) channels (glibenclamide, 10 microM) and prostaglandin synthesis (indomethacin, 10 microM). CHA and NECA induced relaxation of rat-tail artery by 80% and 70% in a concentration-dependent manner, respectively. The relaxation effect of NECA was completely abolished in the presence of L-NAME, while glibenclamide and indomethacin prevented CHA-induced relaxation of the rat tail artery by approximately 25% and 40%, respectively. Our results indicate that nonspecific effects such nitric oxide and prostaglandins release or the activation of potassium channels significantly contributed to the effects of CHA and NECA.
Authors and Affiliations
Katarzyna Kedzior, Renata Szczepańska, Ivan Kocić
Keywords
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