ABSTRACT
The role of gap junctions in EDHF-mediated responses and the mechanisms of K + - induced relaxation have been investigated in the rat isolated mesenteric arterial bed. Endothelium-derived hyperpolarizing factor (EDHF)-mediated responses to carbachol (in the presence of indomethacin and N G -nitro-L-arginine methyl ester ( L - N A M E ) were substantially reduced in the presence the gap junction inhibitors, 18a-glycyrrhetinic acid, SR141716A and palmitoleic acid, and also ouabain and clotrimazole. K + caused dilatations of preparations perfused with K + free buffer, which were sensitive to both ouabain and 18a-glycyrrhetinic acid but not to SR141716A, palmitoleic acid or clotrim azole. The relaxations to K + were reduced following inhibition of cycloxygenase and were abolished by removal of the endothelium. It is concluded that gap junctional communication plays a major role in endothelium-dependent relaxations mediated by E D H F and that K + causes dilatation in an endothelium-dependent manner, which is in part mediated via prostanoids.
