Arterial relaxation mediated by endothelium-derived hyperpolarizing factorin hypertension induced by chronic inhibition of nitric oxide synthesis

The aim of this study was to evaluate arterial relaxation mediated by endot helium-derived hyperpolarizing factor (EDHF) during chronic inhibition of n itric oxide (NO) synthase. We measured the isometric tension of isolated me senteric arteries of Wistar rats administered N-omega-nitro-L-arginine meth yl ester (L-NAME, 100 mg/Kg/day) for 3 weeks. Relaxation to acetylcholine ( ACh) was reduced in L-NAME treated rats (maximum relaxation, 52% versus 79% ). After acute superfuison of 1x10(-4) M L-NAME, half the relaxation was in hibited in controls, while the relaxation was not changed in L-NAME treated rats. In contrast, relaxation to nitroprusside was normal in L-NAME treate d rats. Superfusion of 1x10(-6) M apamin, which inhibits the effects of EDH F, reduced the relaxation. The relaxation inhibited by apamin was not signi ficantly different between the two groups. These findings suggested that in endothelial cells, the synthesis of EDHF is unchanged during a chronic def iciency of relaxation influence of NO.