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

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.

Levosimendan and its metabolite OR-1896 elicit KATP channel-dependent dilation in resistance arteries in vivo

“…At the moment, we do not have a clear-cut explanation for the complexity of levosimendan-induced vascular responses in various vessels and species, and we therefore speculate that the expressions and/or regulations of K ATP and BK Ca channels are not uniform in the investigated vascular preparations [9, 16, 23]. The present results do not support the hypothesis of additional vasodilator mechanisms [21, 26] involving partial mediation of the action of levosimendan and OR-1896 by cAMP.…”

Mechanisms involved in the adenosine-induced vasorelaxation to the pig prostatic small arteries

“…In addition to NO, the COX pathway has also been involved in the vasorelaxations to adenosine [39]. In pig prostatic arteries, indomethacin, a non-selective COX inhibitor, failed to modify the relaxations to NECA, thus excluding a possible role of prostanoids in these responses.…”