| 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 × 10-7 mol l-1) or exposure to a calcium-free medium abolished the spontaneous as well as K+-induced contractions. A^-nitro-L-arginine (10-4 mol l-1), indomethacin (3 × 10-6 mol l-1) and glibenclamide (10-5 mol I-1) did not affect the contractile response to K+ in intact arteries. However, Nw-nitro-D-arginine increased the baseline tension, and this effect could not be reproduced with Nw-nitro-D-arginine. Pinacidil (10-6mol l-l) 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 I-l) increased the basal tension and shifted the K+ concentration-response curve to the left. Calcium-induced contractions in preparations exposed to a calcium-free, 124 mmol l-l K.+ solution did not differ between endothelium-denuded and intact arteries. It is suggested that the endothelium of the rabbit basilar artery releases a hyperpolarizing factor, distinct from nitric oxide or a cyclooxygenase product, which attenuates the vasoconstrictor effect of K+ depolarization. |
