ENDOTHELIUM-DEPENDENT NORADRENALINE-INDUCED RELAXATION OF RAT ISOLATED CEREBRAL-ARTERIES - PHARMACOLOGICAL CHARACTERIZATION OF RECEPTOR SUBTYPES INVOLVED

1 The endothelium-dependence of catecholamine-induced relaxation of rat cerebr 2 In the basilar artery (BA), the maximal relaxant response was most pronounced with noradrenaline (NA), less with isoprenaline (Iso), and only very little with terbutaline. Methoxamine and the alpha2-adrenoceptor selective agonists BHT 933 and clonidine, had no relaxant effect. 3 In BA, the relaxation by NA or Iso was markedly attenuated by N(omega)-nitro-L-arginine (L-NOARG) 10(-4) m. Short term perfusion of the vessels by Triton X 100 (1:1 000) suppressed the NA-induced relaxation. 4 The relaxation induced by NA or Iso was markedly reduced in presence of L-NOARG in the posterior, medial and anterior cerebral artery. 5 In BA, NA-induced relaxation was non-competitively inhibited by propranolol, atenolol, and the beta1- and beta2-adrenoceptor selective antagonists, CGP 20712 A and ICI 118551. 6 The relaxant NA-effect was not affected by prazosin but was non-competitively blocked by phentolamine. 7 The Iso-induced relaxation was competitively blocked by propranolol, whereas atenolol, CGP 20712 A and ICI 118551 caused a non-competitive inhibition. 8 The experiments indicate that the catecholamine-induced relaxation in rat isolated cerebral arteries depends upon the endothelium. They suggest that the NA-induced relaxation of BA is mediated by different alpha- and beta-adrenoceptors and that the Iso-induced relaxation is mediated by different beta-receptors. The findings would also be compatible with the idea of a receptor type which cannot be characterized by the pharmacological tools that we have used.