KATP channels do not mediate vasodilation by 3-morpholinosydnonimine in goat coronary artery

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 6.61×10^?7 M. Methylene blue (3×10^?6 M) caused a rightward shift in the concentration–response curve of SIN-1 (10^?8–3×10^?5 M) with a corresponding increase in the EC₅₀ (3.62×10^?6 M) of the nitrovasodilator. While the K_ATP channel blocker, glibenclamide (1 and 3×10^?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.