Lin H, Young D B
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216-4505, USA.
Am J Physiol. 1997 Sep;273(3 Pt 2):F457-62. doi: 10.1152/ajprenal.1997.273.3.F457.
Results from previous experiments in our laboratory suggested that a H(+)-K(+)-adenosinetriphosphatase (H(+)-K(+)-ATPase) was present in vascular smooth muscle. Here we analyzed the effects on regulation of renal vascular function in anesthetized dogs of inhibition of the H(+)-K(+)-ATPase by a highly specific inhibitor, NC-1300-B. The compound was injected intravenously, 15 mg/kg (5.8 x 10(-5) mol wt/kg), into one group of six dogs, whereas saline was given to a control group of eight. Renal function was measured at controlled levels of renal perfusion pressure ranging from 110 to 60 mmHg. Renal blood flow (RBF) was higher in the treated group at all levels of perfusion pressure; at 70 mmHg, the treated group RBF was 5.85 +/- 1.00 ml.min-1.g kidney wt-1, 71% greater than that of the control group. Glomerular filtration rate (GFR) mean values of the two groups were not significantly different at any perfusion pressure level. Renin release was inhibited (P < 0.01) by H(+)-K(+)-ATPase inhibition; at 90 mmHg, the control group mean was 14.3 +/- 4.3 units, 4.47 times greater than the treated group mean of 3.2 +/- 1.6 units. H(+)-K(+)-ATPase inhibition with NC-1300-B causes profound renal vasodilation and inhibition of renin release without affecting regulation of GFR.
我们实验室先前的实验结果表明，血管平滑肌中存在一种氢钾三磷酸腺苷酶（H(+)-K(+)-ATP酶）。在此，我们分析了一种高度特异性抑制剂NC-1300-B对麻醉犬肾血管功能调节的影响。将该化合物以15mg/kg（5.8×10(-5)mol wt/kg）的剂量静脉注射到一组6只犬中，而另一组8只犬作为对照组给予生理盐水。在110至60mmHg的可控肾灌注压力水平下测量肾功能。在所有灌注压力水平下，治疗组的肾血流量（RBF）均较高；在70mmHg时，治疗组的肾血流量为5.85±1.00ml·min-1·g肾重-1，比对照组高71%。在任何灌注压力水平下，两组的肾小球滤过率（GFR）平均值均无显著差异。氢钾三磷酸腺苷酶抑制可抑制肾素释放（P<0.01）；在90mmHg时，对照组平均值为14.3±4.3单位，是治疗组平均值3.2±1.6单位的4.47倍。用NC-1300-B抑制氢钾三磷酸腺苷酶可导致肾血管显著扩张并抑制肾素释放，而不影响肾小球滤过率的调节。
