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Apelin (AP) is the endogenous ligand of the recently de-orphanized APJ receptor. Despite the highly expression of both AP and APJ in the vascular wall, the vasomotor effects of AP are still under investigation. We have recently shown that AP plays a counter-regulatory role against the angiotensin II -induced vasoconstriction. The aim of this study was to investigate the action of AP (cumulative dose, 1nM - 10_M) on aorta (Ao), pulmonary artery (PA), renal vein (RV) and portal vein (PV) precontracted with phenylephrine (Phe, 10_M) and to what extent, if any, NO mediates the AP effects. Experiments were performed on rat vessels rings with (EI) or without endothelium (ED), in absence or presence of 10_M N(G)-nitro L-arginine methyl ester (L-NAME, NO synthase inhibitor). The NO production was continuously monitored by a NO meter. The AP-induced relaxation were the highest on PV (Emax _ 56.41_3.18%) and the lowest on the Ao intact rings (Emax _ 16.93_6.24%). The absence of intact endothelium or L-NAME pretreatment prevented AP effects on Ao and RV rings. On PA ED rings or on PA EI rings but after L-NAME pretreatment AP effects were still significantly but 2.5 and 1.7 times lower. Blocking NO synthesis decreased AP-induced relaxation of Phe precontracted PV rings, L-NAME being significantly powerful on endothelium denuded (up to 90%) than endothelium intact rings (up to 60%). These results, together with NO measuring, suggested that, depending on vessel type, AP could relax pre-contracted vessels by NO dependent and partially endothelium – independent mechanisms. |
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