Deka D K, Raviprakash V, Mishra S K
Division of Pharmacology and Toxicology, Indian Veterinary Research Institute, Izatnagar.
Eur J Pharmacol. 1997 Jul 9;330(2-3):157-64. doi: 10.1016/s0014-2999(97)00175-1.
The present study investigated the role of ATP-sensitive potassium (K(ATP)) channels in mediating relaxation to the nitric oxide (NO) donor, 3-morpholinosydnonimine (SIN-1) in goat coronary arteries. SIN-1 (10(-8)-10(-5) M) caused concentration-dependent relaxations of the coronary artery ring segments contracted with K+ (30 mM) with an EC50 of 6.61 x 10(-7) M. Methylene blue (3 x 10(-6) M) caused a rightward shift in the concentration-response curve of SIN-1 (10(-8)-3 X 10(-5) M) with a corresponding increase in the EC50 (3.62 x 10(-6) M) of the nitrovasodilator. While the K(ATP) channel blocker, glibenclamide (1 and 3 x 10(-6) M) caused dose-dependent inhibition of vasorelaxations produced by pinacidil (10(-8)-10(-4) M), it had no effect on the vasodilations elicited by SIN-1 (10(-8)-10(-5) M) in the coronary arterial smooth muscle. Increasing the extracellular K+ concentration from 30 mM to 80 mM to reduce the K+ gradient across the cell membrane, inhibited the relaxations elicited by pinacidil (10(-8)-10(-4) M). On the other hand, SIN-1 (10(-8)-10(-5) M)-induced relaxations were potentiated in high K+ (80 mM) compared to those observed at K+ (30 mM). These results suggest that goat coronary artery vasodilations caused by the NO donor, SIN-1, do not involve K(ATP) channels.
