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

The aim of this study was to evaluate arterial relaxation mediated by endothelium-derived hyperpolarizing factor (EDHF) during chronic inhibition of nitric oxide (NO) synthase. We measured the isometric tension of isolated mesenteric arteries of Wistar rats administered Nomega-nitro-L-arginine methyl 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 superfusion of 1x10(-4) M L-NAME, half the relaxation was inhibited in controls, while the relaxation was not changed in L-NAME treated rats. In contrast, relaxation to nitroprusside was normal in L-NAME treated rats. Superfusion of 1x10(-6) M apamin, which inhibits the effects of EDHF, reduced the relaxation. The relaxation inhibited by apamin was not significantly different between the two groups. These findings suggested that in endothelial cells, the synthesis of EDHF is unchanged during a chronic deficiency of relaxation influence of NO.