Gardes J, Poux J M, Gonzalez M F, Alhenc-Gelas F, Menard J
INSERM U36, Paris, France.
Life Sci. 1992;50(14):987-93. doi: 10.1016/0024-3205(92)90092-4.
A possible role of the endothelial L-arginine/NO pathway in the control of renal hemodynamics, renin release and kallikrein secretion was studied in an isolated rat kidney model perfused in a closed-circuit. NG-nitro-L-arginine methyl ester (L-NAME, 1-50 microM), an inhibitor of nitric oxide biosynthesis, caused a dose-dependent increase in perfusion pressure (PP) and a dose-dependent decrease in renal perfusate flow. Renin release was inhibited independently of a rise in PP. L-NAME did not change the urinary kallikrein secretion. These results confirm the intervention of the L-arginine/NO pathway in the vasodilation of this isolated perfused kidney model and demonstrate the inhibitory effect of L-NAME on renin release. They suggest that nitric oxide synthesis plays a role in stimulating renin release and is not involved in the regulation of urinary kallikrein secretion.
在一个闭路灌注的离体大鼠肾脏模型中，研究了内皮型L-精氨酸/一氧化氮途径在控制肾血流动力学、肾素释放和激肽释放酶分泌方面的可能作用。一氧化氮生物合成抑制剂NG-硝基-L-精氨酸甲酯（L-NAME，1-50微摩尔）导致灌注压力（PP）呈剂量依赖性增加，肾灌注液流量呈剂量依赖性减少。肾素释放受到抑制，且与PP升高无关。L-NAME未改变尿激肽释放酶分泌。这些结果证实了L-精氨酸/一氧化氮途径对该离体灌注肾脏模型血管舒张的干预作用，并证明了L-NAME对肾素释放的抑制作用。它们表明一氧化氮合成在刺激肾素释放中起作用，且不参与尿激肽释放酶分泌的调节。
