ENHANCEMENT OF DEPOLARIZATION-INDUCED CONTRACTIONS AFTER ENDOTHELIUM DENUDATION IS NOT RELATED TO AN IMPAIRED PRODUCTION OF NITRIC-OXIDE ORPROSTACYCLIN IN THE RABBIT BASILAR ARTERY

Enhancement of the extracellular potassium ion (K+) concentration comb ined with endothelial injury have been suggested to occur during cereb ral ischaemia-reperfusion and vasospasm after subarachnoid hemorrhage. The effect of potassium (K+) depolarization was therefore investigate d in isolated segments of the rabbit basilar artery with and without a n 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+ conce ntration eliciting half maximum contraction decreased from 26 mmol l(- 1) in the presence to 12 mmol l(-1) in the absence of an intact endoth elium. 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 con tractile response to K+ in intact arteries. However, N-omega-nitro-L-a rginine increased the baseline tension, and this effect could not be r eproduced 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-resp onse curve to the left. Calcium-induced contractions in preparations e xposed to a calcium-free, 124 mmol l(-1) K+ solution did not differ be tween endothelium-denuded and intact arteries. It is suggested that th e 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.