Contribution of NO, ATP-sensitive K+ channels and prostaglandins to adenosine receptor agonists-induced relaxation of the rat tail artery.

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.