Hannedouche T, Schmitt F, Ikeni A, Marques L P, Natov S, Déchaux M, Lacour B, Grünfeld J P
Department of Nephrology, Hôpital Necker, Paris, France.
Hypertension. 1993 Mar;21(3):261-6. doi: 10.1161/01.hyp.21.3.261.
In 13 normotensive subjects on a normal sodium diet, we studied hormonal, blood pressure, and renal vascular changes and dextran sieving profiles induced by infusion of exogenous angiotensin II (Ang II) (5 ng.kg-1.min-1). during baseline conditions and after 5 days of administration of the angiotensin converting enzyme inhibitor cilazapril. Cilazapril induced a renal vasodilative effect without affecting supine blood pressure and glomerular filtration rate. Fractional dextran clearances were significantly decreased for dextran of effective radius ranging from 3.0 to 4.0 nm. This shift was primarily related to an increase in glomerular capillary plasma flow, because no change was observed in the transcapillary glomerular pressure gradient, the ultrafiltration coefficient, or the membrane parameters. Ang II elicited a slight pressor response accompanied by hormonal, antinatriuretic, and renal hemodynamic changes that were similar during and before short-term angiotensin converting enzyme inhibition. Dextran sieving curves were unchanged by a low dose of Ang II. However, the transcapillary glomerular pressure gradient and the ultrafiltration coefficient were computed to increase by 19.4% and to decrease by 44.2%, respectively, whereas membrane parameters were unaffected. When superimposed onto short-term angiotensin converting enzyme inhibition, glomerular response to this unique dose of Ang II was similar to that induced by Ang II alone. These findings indirectly suggest that most, if not all, of the renal effects of cilazapril are mediated through suppression of Ang II formation.
在13名正常钠饮食的血压正常受试者中，我们研究了外源性输注血管紧张素II（Ang II）（5 ng·kg⁻¹·min⁻¹）在基线条件下以及给予血管紧张素转换酶抑制剂西拉普利5天后所诱发的激素、血压、肾血管变化以及葡聚糖筛过情况。西拉普利诱导了肾血管舒张作用，而不影响仰卧位血压和肾小球滤过率。有效半径在3.0至4.0 nm之间的葡聚糖的分数清除率显著降低。这种变化主要与肾小球毛细血管血浆流量增加有关，因为跨毛细血管肾小球压力梯度、超滤系数或膜参数均未观察到变化。Ang II引起轻微的升压反应，同时伴有激素、抗利钠和肾血流动力学变化，在短期血管紧张素转换酶抑制期间和之前相似。低剂量的Ang II未改变葡聚糖筛过曲线。然而，计算得出跨毛细血管肾小球压力梯度增加了19.4%，超滤系数降低了44.2%，而膜参数未受影响。当叠加短期血管紧张素转换酶抑制时，肾小球对这一特定剂量Ang II的反应与单独使用Ang II时相似。这些发现间接表明，西拉普利的大多数（如果不是全部）肾脏效应是通过抑制Ang II的形成介导的。
