Endothelium‐dependent noradrenaline‐induced relaxation of rat isolated cerebral arteries: pharmacological characterization of receptor subtypes involved

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Abstract
1 The endothelium-dependence of catecholamine-induced relaxation of rat cerebral arteries was investigated in vitro. 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 α2-adrenoceptor selective agonists BHT 933 and clonidine, had no relaxant effect. 3 In BA, the relaxation by NA or Iso was markedly attenuated by Nω-nitro-l-arginine (l-NOARG) 10−4 m. Short term perfusion of the vessels by Triton X 100 (1:1000) 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 β1- and β2-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 α- and β-adrenoceptors and that the Iso-induced relaxation is mediated by different β-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.