ABSTRACT
In several blood vessels, endothelium-dependent relaxations are in part mediated by an endothelium-derived hyperpolarizing factor ( E D H F ) , the nature of which is unknown. Experiments were performed to investigate the hypothesis that in small gastric arteries of the rat E D H F might be identified as potassium ions, released by activation of endothelial K C a -channels and inducing relaxation by stimulation of N a + / K + - p u m p and the inward rectifier K + conductance. EDHF-induced relaxations (assessed as the nitroL-arginine/indomethacin resistant component of acetylcholine-induced relaxations of preparations contracted with norepinephrine), but not sodium nitroprusside-induced relaxations are inhibited in the presence of ouabain plus B a 2 + . Ouabain is responsible for the greater part of the inhibition. This inhibition is reversible. Application of increasing concentrations of K + elicits in some preparations transient relaxations, but in a greater part of the preparations, there are no or only small relaxations. The K C a -channel opener N S 1619 elicits relaxation effects that are not diminished after removal of the endothelium and are not inhibited by ouabain plus B a 2 + . Similar results are obtained with 1-EBIO, a K C a -channel opener acting more selectively on endothelial cells. Thus, EDHF-mediated relaxation is sensitive to inhibition by ouabain plus B a 2 + , but the relation of this inhibitory influence to an action of K + as E D H F is unlikely.
