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.

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)