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

The effect of K+ channel blockers on acetylcholine-induced relaxation in guinea-pig uterine arterial rings was investigated. Acetylcholine (0.1 nM-60 microM) induced endothelium-dependent relaxation of phenylephrine-precontracted guinea-pig uterine artery. Methylene blue (30 nM-1 microM) and NG-monomethyl-L-arginine (3-30 microM) antagonized the effect of acetylcholine, with suppression of the maximal acetylcholine-induced relaxation, in a concentration-dependent manner. The inhibition of relaxation by NG-monomethyl-L-arginine (10 microM) was significantly overcome by L-arginine (10 microM), but not by D-arginine (100 microM). In contrast, the administration of K+ channel blockers, tetraethylammonium (6 mM), glibenclamide (5 microM), apamin (1 microM) 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 NG-monomethyl-L-arginine (30 microM). Finally, the acetylcholine-evoked relaxations were unaltered when K(+)-rich Krebs-Ringer-bicarbonate solution was used to induce tone instead of phenylephrine. Indomethacin (10 microM) and diethylcarbamazine (100 microM) 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.