Phorbol ester and central chemosympathectomy augment beta-adrenoceptor response by different mechanisms

• Authors: Irena Nalepa , Jerzy Vetulani
• Languages of publication: EN

Abstracts

EN

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.

Keywords

EN

6-HYDROXYDOPAMINE; ADRENOCEPTOR; CYCLIC AMP

Discipline

• PHARMACOLOGY: PHARMACOLOGY

• Publisher: Institute of Pharmacology, Polish Academy of Sciences
• Journal: Polish Journal of Pharmacology
• Year: 1993
• Volume: 45
• Issue: 2
• Pages: 167-175

Contributors

author

Irena Nalepa

author

Jerzy Vetulani

• Document Type: article