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

• Published in: European journal of pharmacology 1995-06, Vol.280 (1), p.95-100
• Main Authors: JOVANOVIC, A, GRBOVIC, L, JOVANOVIC, S
• Format: Article
• Language: English
• Subjects: Acetylcholine; Acetylcholine - pharmacology; Animals; Arginine - analogs & derivatives; Arginine - pharmacology; Arteries - drug effects; Arteries - physiology; Biological and medical sciences; Blood vessels and receptors; Diethylcarbamazine - pharmacology; Drug Interactions; Endothelium; Female; Fundamental and applied biological sciences. Psychology; Guinea Pigs; In Vitro Techniques; Indomethacin - pharmacology; Isotonic Solutions - pharmacology; K + channel blocker; Methylene Blue - pharmacology; Muscle Relaxation - drug effects; Muscle, Smooth, Vascular - drug effects; Muscle, Smooth, Vascular - physiology; Nitric oxide (NO); omega-N-Methylarginine; Potassium Channels - drug effects; Potassium Channels - physiology; Uterine artery; Uterus - blood supply; Vertebrates: cardiovascular system
• ISSN: 0014-2999; 1879-0712
• DOI: 10.1016/0014-2999(95)00236-E

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.