Evidence that A(2a) and not A(2b) purinoceptors are coupled to production of nitric oxide in the central regulation of blood pressure

L Stella; V de Novellis; L Berrino; M D'Amico; F Rossi

doi:10.1016/s1382-6689(96)00065-8

Evidence that A(2a) and not A(2b) purinoceptors are coupled to production of nitric oxide in the central regulation of blood pressure

Environ Toxicol Pharmacol. 1996 Dec 20;2(4):327-9. doi: 10.1016/s1382-6689(96)00065-8.

Authors

L Stella¹, V de Novellis, L Berrino, M D'Amico, F Rossi

Affiliation

¹ Institute of Pharmacology and Toxicology, Faculty of Medicine and Surgery, 2nd University of Naples, Via Broggia 3, 80138 Naples, Italy.

PMID: 21781738
DOI: 10.1016/s1382-6689(96)00065-8

Abstract

In a previous study we reported that nitric oxide (NO) partially mediates centrally the decrease of arterial blood pressure induced by adenosine A(2) subtype receptor stimulation. The present study confirms the earlier suggestion and shows that in adult male normotensive anaesthetized rats 5'-N-ethylcarboxamidoadenosine (NECA), a non-selective adenosine receptor agonist, centrally injected induced a significant decrease of arterial blood pressure. Moreover, the observation that intracerebroventricular (i.c.v.) administration of N(ω)-nitro-l-arginine methyl ester (l-NAME), a NO synthase inhibitor, +8-(3-chlorostyryl)-caffeine (CSC), antagonist of A(2a) receptors, did not reduce furthermore the hypotensive effect induced by NECA injection, demonstrated that NO is involved only via A(2a) and not via A(2b) adenosine subtype receptors in the central regulation of blood pressure.