title: K(ATP) channels do not mediate vasodilation by 3-morpholinosydnonimine in goat coronary artery.
abstract: 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.
authors.affiliation: Division of Pharmacology and Toxicology, Indian Veterinary Research Institute, Izatnagar.
authors.forename: D K
authors.initials: DK
authors.lastname: Deka
authors.forename: V
authors.initials: V
authors.lastname: Raviprakash
authors.forename: S K
authors.initials: SK
authors.lastname: Mishra
mesh_terms: D000255:Adenosine Triphosphate / Q000502:physiology*; D000818:Animals; D003331:Coronary Vessels / Q000187:drug effects / Q000502:physiology*; D005905:Glyburide / Q000494:pharmacology; D006041:Goats; D006146:Guanidines / Q000494:pharmacology; D007004:Hypoglycemic Agents / Q000494:pharmacology; D066298:In Vitro Techniques; D008981:Molsidomine / Q000031:analogs & derivatives* / Q000494:pharmacology; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology; D020110:Pinacidil; D011188:Potassium / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*; D014665:Vasodilator Agents / Q000494:pharmacology*
chemical_list: D006146:Guanidines; D007004:Hypoglycemic Agents; D015221:Potassium Channels; D013757:Tetraethylammonium Compounds; D014665:Vasodilator Agents; C002385:linsidomine; D019789:Tetraethylammonium; D020110:Pinacidil; D000255:Adenosine Triphosphate; D008981:Molsidomine; D011188:Potassium; D005905:Glyburide