Influence of aortic baroreceptor denervation on adenosine receptor-mediated relaxation of isolated rat aorta

Abstract

The effect of aortic baroreceptor denervation on the vasorelaxant activity of the adenosine analogue, 5′-N-ethylcarboxamidoadenosine (NECA) was evaluated in the isolated thoracic aortic rings from rats. The responses were evaluated at 3 h after baroreceptor denervation when the blood pressure was significantly higher than that of control (149±3 vs. 112±2 mmHg) and at 48 h after aortic baroreceptor denervation when blood pressure returned to control level. Sham operation had no effect on blood pressure at either time interval. A concentration-dependent relaxation of rat aorta elicited by NECA was observed in all groups. However, the responsiveness to NECA was reduced in aortic baroreceptor-denervated rats. The nitric oxide (NO) synthase inhibitor, L-monomethyl- L-arginine (30 μM) shifted the dose-response curve for NECA to the right in all groups suggesting that the vascular response to NECA is partially mediated through the release of NO. Removal of the endothelium abolished the differences in the response to NECA in sham and aortic baroreceptor-denervated rats suggesting that the decrease in the responsiveness of aortic smooth muscle to NECA is dependent on the release of NO. Vasorelaxant responses to acetylcholine were not altered by aortic baroreceptor denervation. The ability of aortic baroreceptor denervation to attenuate vasorelaxant responses to NECA but not to acetylcholine indicated the possibility of functional changes involving adenosine receptor-mediated relaxation in endothelium rather than structural changes due to aortic baroreceptor denervation. These findings suggest that short-term elevation of blood pressure following aortic baroreceptor denervation modulates the endothelium-dependent release of NO mediated by adenosine receptor activation.