Neisius D, Wood J M, Hofbauer K G
Am J Physiol. 1986 Nov;251(5 Pt 2):H897-902. doi: 10.1152/ajpheart.1986.251.5.H897.
The relative importance of angiotensin II for the renal vasodilatory response after converting-enzyme inhibition was evaluated by a comparison of the effects of converting-enzyme and renin inhibition on renal vascular resistance. Renal, mesenteric, and hindquarter blood flows were measured with chronically implanted ultrasonic-pulsed Doppler flow probes in conscious, mildly volume-depleted marmosets after administration of a converting-enzyme inhibitor (enalaprilat, 2 mg/kg iv), a synthetic renin inhibitor (CGP 29,287, 1 mg/kg iv), or a renin-inhibitory monoclonal antibody (R-3-36-16, 0.1 mg/kg iv). Enalaprilat reduced blood pressure (-16 +/- 4 mmHg, n = 6) and induced a selective increase in renal blood flow (27 +/- 8%, n = 6). CGP 29,287 and R-3-36-16 induced comparable reductions in blood pressure (-16 +/- 4 mmHg, n = 6 and -20 +/- 4 mmHg, n = 5, respectively) and selective increases in renal blood flow (36 +/- 12%, n = 6 and 34 +/- 16%, n = 4, respectively). The decrease in renal vascular resistance was of similar magnitude for all of the inhibitors (enalaprilat -28 +/- 3%, CGP 29,287 -32 +/- 6%; and R-3-36-16 -33 +/- 7%). These results indicate that the renal vasodilatation induced after converting-enzyme or renin inhibition is mainly due to decreased formation of angiotensin II.
通过比较转化酶抑制和肾素抑制对肾血管阻力的影响，评估了血管紧张素II在转化酶抑制后肾血管舒张反应中的相对重要性。在清醒、轻度容量不足的狨猴中，使用长期植入的超声脉冲多普勒血流探头测量肾、肠系膜和后肢血流量，这些狨猴在给予转化酶抑制剂（依那普利拉，2mg/kg静脉注射）、合成肾素抑制剂（CGP 29,287，1mg/kg静脉注射）或肾素抑制性单克隆抗体（R-3-36-16，0.1mg/kg静脉注射）后。依那普利拉降低了血压（-16±4mmHg，n=6），并引起肾血流量选择性增加（27±8%，n=6）。CGP 29,287和R-3-36-16引起了类似的血压降低（分别为-16±4mmHg，n=6和-20±4mmHg，n=5）和肾血流量选择性增加（分别为36±12%，n=6和34±16%，n=4）。所有抑制剂引起的肾血管阻力降低幅度相似（依那普利拉-28±3%，CGP 29,287-32±6%；R-3-36-16-33±7%）。这些结果表明，转化酶或肾素抑制后诱导的肾血管舒张主要是由于血管紧张素II生成减少。
