Bergström G, Rudenstam J, Creutz J, Göthberg G, Karlström G
Institute of Physiology and Pharmacology, Department of Physiology, University of Göteborg, Sweden.
Acta Physiol Scand. 1995 Jun;154(2):241-52. doi: 10.1111/j.1748-1716.1995.tb09906.x.
Blockade of NO synthesis with N-omega-nitro-L-arginine (L-NNA) inhibits the vasodepressor response seen in intact Wistar assay rats in which isolated kidneys perfused via an extracorporeal circuit are perfused at high pressure. This study explores the renal and haemodynamic changes associated with this inhibition. Isolated kidneys (IK) were perfused at high pressure (175 mmHg) by a pump in series with intact Wistar assay rats in which blood pressure (BP), haemodynamics and renal function were studied. Nitric oxide (NO) synthesis was blocked by L-NNA (2.5 mg kg-1) in 13 experiments (175NO) while 14 control experiments (175C) were performed. IK was perfused at 90 mmHg in seven experiments (90C). The BP drop in the 175C assay rat was blocked by L-NNA in 175NO (P < 0.01). However, when the blockade was reversed with L-arginine infusion (20 mg kg-1 min-1) BP declined also in 175NO. Effective renal plasma flow (ERPF) and glomerular filtration rate (GFR) fell dramatically after L-NNA in both the assay rat and in IK despite a high perfusion pressure. The marked increase in filtration fraction (FF) after L-NNA suggests a dominating postglomerular vasoconstriction. The natriuretic response in IK to 175 mmHg was also markedly blunted by L-NNA. We conclude that NO blockade inhibits the renomedullary depressor mechanism probably by restricting renal blood flow, and also blunts the pressure induced natriuretic response as a result of a reduced sodium filtration. Finally, the autoregulation of whole kidney blood flow seems to be more efficient although set at a higher level of vasoconstriction.
用N-ω-硝基-L-精氨酸（L-NNA）阻断一氧化氮（NO）合成可抑制完整Wistar实验大鼠中出现的血管降压反应，在这些大鼠中，通过体外循环灌注的离体肾脏处于高压灌注状态。本研究探讨了与此种抑制相关的肾脏和血流动力学变化。将离体肾脏（IK）与完整的Wistar实验大鼠串联用泵进行高压（175 mmHg）灌注，同时研究大鼠的血压（BP）、血流动力学和肾功能。在13个实验（175NO）中，用L-NNA（2.5 mg kg-1）阻断NO合成，同时进行14个对照实验（175C）。在7个实验（90C）中，IK以90 mmHg进行灌注。L-NNA可阻断175C实验大鼠中的BP下降（P < 0.01）。然而，当用L-精氨酸输注（20 mg kg-1 min-1）逆转阻断时，175NO中的BP也下降。尽管灌注压力较高，但在实验大鼠和IK中，L-NNA作用后有效肾血浆流量（ERPF）和肾小球滤过率（GFR）均显著下降。L-NNA作用后滤过分数（FF）的显著增加提示肾小球后血管收缩占主导。L-NNA也显著减弱了IK对175 mmHg的利钠反应。我们得出结论，NO阻断可能通过限制肾血流量抑制肾髓质降压机制，并且由于钠滤过减少也减弱了压力诱导的利钠反应。最后，尽管设定在较高的血管收缩水平，但全肾血流的自身调节似乎更有效。
