Lack of interaction between alpha(2)-autoreceptors and prejunctional receptors mediating a facilitatory effect on noradrenaline release

• Type: Article in International Scientific Journal
• Date: 2000

Authors

Alberto Mota (Author) FMUP; Paiva, MQ (Author) Other; moura, d (Author) FMUP; Guimaraes, S (Author) Other

Journal

Title: Pharmacological Research

Vol. 42

Pages: 383-387

ISSN: 1043-6618

Publisher: Elsevier

Indexing

ISI Web of Knowledge - 9 Citations

Scopus - 8 Citations

Other information

Authenticus ID: P-000-YXJ

DOI: 10.1006/phrs.2000.0707

Abstract (EN): The present study was undertaken to investigate the effect of alpha(2)-autoreceptor blockade on the facilitatory influence exerted by activation of beta-, A(2A)-adenosine- and angiotensin II receptors. Segments of a rat-tail artery, previously incubated with H-3-noradrenaline, were subjected to electrical stimulation. The influence of isoprenaline, the compound CGS21680 and angiotensin II on the overflow of tritium evoked by electrical stimulation was checked before and after alpha(2)-adrenoceptor blockade. All the agonists used caused concentration-dependent increases of tritium overflow, the maximal effect representing increases of 44.2, 27.4 and 41.2% for isoprenaline, CGS21680 and angiotensin II, respectively. In the presence of alpha(2)-adrenoceptor blockade by phenoxybenzamine (1 mu M) or yohimbine (33 or 100 nM), the facilitatory influence of isoprenaline, CGS21680 and angiotensin II was not significantly changed. Since this facilitatory influence, which involves the activation of G(s)- or G(q)-proteins, was not enhanced by alpha(2)-adrenoceptor blockade, it is concluded that the enhancement of the negative modulation resulting from activation of A(1)-adenosine-, muscarine- and kappa-receptors, as previously shown, should be due to the fact that the involved systems share signal transduction mechanisms, or at least G-proteins. (C) 2000 Academic Press.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 5