Phorbol ester and central chemosympathectomy augment beta-adrenoceptor response by different mechanisms
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The aim of this study was to compare the mechanisms of increased responsiveness of the beta-adrenoceptor dependent cyclic AMP generating system induced by chronic decrease of noradrenaline availability (beta-upregulation) with that resulting from simultaneous stimulation of alfa-adrnoceptors (alfa-potentiation) and to assess the role of portein kinase C in these phenomena. The beta-upregulation was produced by central chemosympathectomy with 6-hydroxydopamine>. The role of alfa1- and alfa2-adrenoceptors was assessed by comparison of the effects of specific beta-adrenoceptor agonist isoproterenol with those of a mixed alfa-beta-adrenoceptor agonist noradrenaline and clonidine was used to selectively stimulate alfa1-adrenoceptors. The role of protein kinase C was assessed by measuring cyclic AMP responses in the presence and absence of 12-O-tetradecanoyl-phorbol 13-acetate. The results indicate that the mechanism of increased responsiveness induced by central chemosympathectomy is different from the alfa-potentiation, that only alfa1-adrenoceptors are involved positively in alfa-potentiation, while the alfa1-adrenoceptors play an inhibitory role, and that increased responsiveness following central chemosympathectomy may be inhibited by protein kinase C activation.
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