흰쥐에서 Nitric oxide 합성억제가 심방이뇨 호르몬의 감압효과에 미치는 영향
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- It has been suggested that nitric oxide (NO) and atrial natriuretic peptide (ANP) share a final common pathway in vascular smooth muscle relaxation. The aim of the present study was to determine the role of NO on the hypotensive and vasorelaxant effect of ANP. Mean arterial pressure and heart rate were continuously recorded from the femoral artery in anesthetized rats and thoracic aortae were mounted in tissue baths to measure the isometric tension. Intravenous administration of ANP (5 ug/kg bolus and 0.2 ug/kg/min infusion) caused a decrease in mean arterial pressure without significant alterations in heart rate. L-NAME-pretreatment (1 mg/kg) suppressed the depressor response to ANP. ANP caused a dose-dependent relaxation in rat aortic rings precontracted with phenylephrine ( 10^(-6) M). The relaxation response to ANP was attenuated by L-NAME (10^(-4) M). Endothelium removal or methylene blue (10^(-5) M) also inhibited the ANP-induced vascular relaxation. The vasorelaxation response to sodium nitroprusside remained unaltered, irrespective of whether endothelium was present or absent. These results suggest that the hypotensive and the vasorelaxant effect of ANP, at least in part, are NO-dependent.
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