K + channel blockers do not modify relaxation of guinea-pig uterine artery evoked by acetylcholine

Abstract

The effect of K + channel blockers on acetylcholine-induced relaxation in guinea-pig uterine arterial rings was investigated. Acetylcholine (0.1 nM-60 μM) induced endothelium-dependent relaxation of phenylephrine-precontracted guinea-pig uterine artery. Methylene blue (30 nM-1 μM) and N G-monomethyl- l-arginine (3–30 μM) antagonized the effect of acetylcholine, with suppression of the maximal acetylcholine-induced relaxation, in a concentration-dependent manner. The inhibition of relaxation by N G-monomethyl- l-arginine (10 μM) was significantly overcome by l-arginine (10 μM), but not by d-arginine (100 μM). In contrast, the administration of K + channel blockers, tetraethylammonium (6 mM), glibenclamide (5 μM), apamin (1 μM) and 4-aminopyridine (1 mM), did not modify the relaxation of guinea-pig uterine artery induced by acetylcholine. The concomitant addition of K + channel blockers in the same concentrations also did not alter the inhibition of acetylcholine-induced relaxation produced by N G-monomethyl- l-arginine (30 μM). Finally, the acetylcholine-evoked relaxations were unaltered when K +-rich Krebs-Ringer-bicarbonate solution was used to induce tone instead of phenylephrine. Indomethacin (10 μM) and diethylcarbamazine (100 μM) had no effects on acetylcholine-induced relaxation. These findings indicate that K + channels are probably not involved in the endothelium-dependent guinea-pig uterine arterial relaxation elicited by acetylcholine.