ROLE FOR ADENOSINE A(1) AND A(2) RECEPTORS IN FEMORAL VASODILATATION INDUCED BY INTRAARTERIAL ADENOSINE IN RABBITS

Citation
K. Sakai et al., ROLE FOR ADENOSINE A(1) AND A(2) RECEPTORS IN FEMORAL VASODILATATION INDUCED BY INTRAARTERIAL ADENOSINE IN RABBITS, European journal of pharmacology, 353(2-3), 1998, pp. 257-264
Citations number
20
Categorie Soggetti
Pharmacology & Pharmacy
ISSN journal
00142999
Volume
353
Issue
2-3
Year of publication
1998
Pages
257 - 264
Database
ISI
SICI code
0014-2999(1998)353:2-3<257:RFAAAA>2.0.ZU;2-8
Abstract
The vasodilator effects of adenosine injected into the femoral artery (i.a.) of rabbits were analyzed. Single bolus i.a. doses of adenosine (0.3-10 mu g) and 5'-(N-cyclopropyl)-carboxamidoadenosine (CPCA)(0.03- 1 mu g), an adenosine A(2)-receptor agonist, produced dose-dependent i ncreases in femoral blood flow and decreases in resistance, almost wit hout affecting blood pressure, heart rate, left ventricular (LV) press ure, and LVdP/dt max, even though CPCA elicited slight decreases in ar terial blood pressure and LV pressure. On the other hand, bolus i.a. i njections of N-6-cyclopentyladenosine (CPA) (1-30 mu g), an adenosine A(1) receptor agonist, caused a relatively weak increase in blood flow , but markedly affected cardiac parameters, especially heart rate and LVdP/dt max. I.v. treatment with 3,7-dimethyl-1-propargylxanthine (DMP X)(2 mg kg(-1)), an antagonist of adenosine A(2) receptors, or 8-pheny ltheophylline (1 mg kg(-1)), an antagonist of adenosine A(2) receptors , significantly attenuated the vasodilator response to adenosine, but not that to acetylcholine. Decreases in blood pressure, heart rate, LV pressure, LVdP/dt max and femoral vascular resistance, and increases in the blood flow elicited by CPA were not significantly modified by t he DMPX treatment, but when this was combined with 8-phenyltheophyllin e, the responses to CPA were completely abolished. The present results indicate that the adenosine-induced femoral vasodilatation in rabbits may be mediated throughout activation of both adenosine A(1) and A(2) receptors. (C) 1998 Elsevier Science B.V. All rights reserved.