Adenosine A(2A) receptor-mediated facilitation of noradrenaline release involves protein kinase C activation and attenuation of presynaptic inhibitory receptor-mediated effects in the rat vas deferens

• Type: Article in International Scientific Journal
• Date: 2003

Authors

Queiroz, G (Author) FFUP; Talaia, C (Author) Other; Goncalves, J (Author) FFUP

Journal

Title: Journal of Neurochemistry

Vol. 85

Pages: 740-748

ISSN: 0022-3042

Publisher: Wiley-Blackwell

Indexing

ISI Web of Knowledge - 19 Citations

Scopus - 23 Citations

Scientific classification

FOS: Medical and Health sciences > Basic medicine

Other information

Authenticus ID: P-000-GWV

DOI: 10.1046/j.1471-4159.2003.01715.x

Abstract (EN): In the epididymal portion of rat vas deferens, facilitation of noradrenaline release mediated by adenosine A(2A) receptors, but not that mediated by beta(2)-adrenoceptors or by direct activation of adenylyl cyclase, was attenuated by blockade of alpha(2)-adrenoceptors and abolished by simultaneous blockade of alpha(2)-adrenoceptors, adenosine A(1) and P2Y receptors. The adenosine A(2A) receptor-mediated facilitation was not changed by inhibitors of protein kinase A, protein kinase G or calmodulin kinase II but was prevented by inhibition of protein kinase C with chelerythrine or bisindolylmaleimide XI. Activation of protein kinase C with phorbol 12-myristate 13-acetate caused a facilitation of noradrenaline release that was abolished by bisindolylmaleimide XI and reduced by antagonists of alpha(2)-adrenoceptors, adenosine A(1) and P2Y receptors. Activation of adenosine A(2A) receptors attenuated the inhibition of noradrenaline release mediated by the presynaptic inhibitory receptors. This effect was mimicked by phorbol 12-myristate 13-acetate and prevented by bisindolylmaleimide XI. It is concluded that adenosine A(2A) receptors facilitate noradrenaline release by a mechanism that involves a protein kinase C-mediated attenuation of effects mediated by presynaptic inhibitory receptors, namely alpha(2)-adrenoceptors, adenosine A(1) and P2Y receptors.

Language: English

Type (Professor's evaluation): Scientific