Potassium channels activated in the endothelium-dependent hyperpolarization in guinea-pig coronary artery

摘要: 1 Properties of the endothelium-dependent hyperpolarization evoked by acetylcholine (ACh) in smooth muscle guinea-pig coronary artery were investigated using conventional microelectrode techniques. 2 ACh hyperpolarized membrane an manner. The comprised two components: initial and a slow hyperpolarization. former appeared during application ACh, while latter occurred after withdrawal ACh. 3 Indomethacin diclofenac, inhibitors enzyme cyclo-oxygenase, blocked only hyperpolarization, indicating that this potential was produced endothelial prostanoids. 4 Clotrimazole SKF 525a, known cytochrome P450, inhibited both hyperpolarizations, suggesting these chemicals acted as non-selective arachidonic acid metabolism. Inhibition lipoxygenase pathway metabolism nordihydroguaiaretic had no effect on either component hyperpolarization. 5 The 4-aminopyridine (4-AP; 10−4-10−3 M) glibenclamide (10−6 M). greatly charybdotoxin (CTX; 5 × 10−8 partially apamin (10−7 M), but not (10−5 Ba2+ (10−4 depolarized increased amplitude components ACh-induced hyperpolarization. 6 Hyperpolarizations Y-26763, K+ channel opener, glibenclamide, 4-AP. 7 The results indicate is prostanoids through activation 4-AP-sensitive channels (possibly delayed rectifier type). mainly CTX-sensitive Ca2+-sensitive