Gardes J, Gonzalez M F, Alhenc-Gelas F, Ménard J
Institut National de la Santé et de la Recherche Médicale U367, Paris, France.
Am J Physiol. 1994 Nov;267(5 Pt 2):F798-804. doi: 10.1152/ajprenal.1994.267.5.F798.
The intervention of the L-arginine-NO pathway in renal vasodilation and renin secretion was studied in an isolated perfused rat kidney model. NG-nitro-L-arginine methyl ester (L-NAME, 1-25 microM), an inhibitor of nitric oxide (NO) synthesis, caused a dose-dependent increase in perfusion pressure (PP) and a dose-dependent decrease in renal perfusate flow. Renin was inhibited independently of the rise in PP, since the effect of L-NAME on renin release was the same when PP was maintained constant. Exposure of rats to low [salt depleted (SD)] or high [salt repleted (SR)] salt intake for 1 mo influenced the renal vascular response to L-NAME (3 microM). Isolated SR rat kidney vasculature vasoconstricted to a greater extent after inhibition of NO synthase than did that of SD kidneys. A similar fall in renin release was observed after L-NAME in both groups, despite a higher renin secretion rate in SD than in SR rats. These results suggest that NO-dependent vasodilation counteracts the renal vasoconstrictor effect of sodium loading.
在离体灌注大鼠肾脏模型中研究了L-精氨酸-一氧化氮途径对肾血管舒张和肾素分泌的干预作用。一氧化氮（NO）合成抑制剂NG-硝基-L-精氨酸甲酯（L-NAME，1 - 25微摩尔）可引起灌注压力（PP）呈剂量依赖性升高以及肾灌注液流量呈剂量依赖性降低。肾素受到抑制，且与PP升高无关，因为当PP保持恒定时，L-NAME对肾素释放的作用相同。将大鼠置于低[缺盐（SD）]或高[补盐（SR）]盐摄入环境中1个月，会影响肾脏血管对L-NAME（3微摩尔）的反应。与SD组肾脏相比，抑制NO合酶后，离体SR组大鼠肾脏血管的收缩程度更大。尽管SD组大鼠的肾素分泌率高于SR组，但两组在给予L-NAME后肾素释放均出现类似程度的下降。这些结果表明，依赖NO的血管舒张作用可抵消钠负荷引起的肾血管收缩效应。
