Enhancement of depolarization‐induced contractions after endothelium denudation is not related to an impaired production of nitric oxide or prostacyclin in the rabbit basilar artery

Abstract

Enhancement of the extracellular potassium ion (K+) concentration combined with endothelial injury have been suggested to occur during cerebral ischaemia-reperfusion and vasospasm after subarachnoid hemorrhage. The effect of potassium (K+) depolarization was therefore investigated in isolated segments of the rabbit basilar artery with and without an intact endothelial cell layer. Addition of potassium chloride to the organ bath induced a concentration-dependent contraction. Endothelial denudation of the artery resulted in an unstable baseline tension and a leftward shift of the K+ concentration-response curve. The K+ concentration eliciting half maximum contraction decreased from 26 mmol l-1 in the presence to 12 mmol l-1 in the absence of an intact endothelium. Nimodipine (3 x 10(-7) mol l-1) or exposure to a calcium-free medium abolished the spontaneous as well as K(+)-induced contractions. N omega-nitro-L-arginine (10(-4) mol l-1), indomethacin (3 x 10(-6) mol l-1) and glibenclamide (10(-5) mol l-1) did not affect the contractile response to K+ in intact arteries. However, N omega-nitro-L-arginine increased the baseline tension, and this effect could not be reproduced with N omega-nitro-D-arginine. Pinacidil (10(-6) mol l-1) abolished the spontaneous contractile activity in endothelium-denuded arteries and reduce the K+ sensitivity to the same level as in intact arteries. Tetraethylammonium (3 mmol l-1) and ouabain (10(-5) mol l-1) increased the basal tension and shifted the K+ concentration-response curve to the left.(ABSTRACT TRUNCATED AT 250 WORDS)