Role of kinins and angiotensin II in the renal hemodynamic response to captopril.
Role of kinins and angiotensin II in the renal hemodynamic response to captopril.
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激肽和血管紧张素 II 在卡托普利肾血流动力学反应中的作用。
DOI：
10.1152/ajprenal.1991.260.5.f670
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Roman,RJ
中科院分区：
文献类型：
--
作者：
Mattson,DL;Roman,RJ
本研究在血浆肾素活性升高的Munich-Wistar大鼠[18.8 +/- 3.3 ng血管紧张素I（ANG I）.ml-1.h-1]中检测了血管紧张素II（ANG II）、激肽和肾上腺素在对卡托普利的肾血流动力学反应中的作用。通过肾脏去神经消除对肾脏的神经影响，并使用主动脉上的夹钳控制肾脏灌注压（RPP）。静脉注射卡托普利（2 mg/kg）后，尿流量、钠排泄量、肾血流量（RBF）、肾小球滤过率（GFR）、皮质和乳头状红细胞（RBC）流量显著增加。肾小球和管周毛细血管压力上升了20%，直小血管毛细血管压力下降了3-4 mmHg，这是由于估计的肾小球前、传出小动脉和肾毛细血管-静脉血管阻力显著降低。输注ANG II（20 ng.kg-1. min-1 iv）使RBF、GFR、肾小球和管周毛细血管压恢复至对照水平;然而，ANG II在抑制前列腺素合成之前并未降低乳头状红细胞流量。Saralasin对乳头状红细胞流量或对卡托普利的反应没有影响。开搏普利引起的直小血管血流动力学变化可被激肽拮抗剂阻断。这些研究结果表明，血管紧张素II对慕尼黑-Wistar大鼠的肾皮质血管系统产生血管收缩作用;然而，其对延髓循环的影响与血管舒张性类花生酸相反。他们还表明，激肽参与了乳头状红细胞流动反应的卡托普利，可能是通过减少流出阻力从直血管循环。
This study examined the role of angiotensin II (ANG II), kinins, and prostaglandins in the renal hemodynamic response to captopril in Munich-Wistar rats in which plasma renin activity was elevated [18.8 +/- 3.3 ng angiotensin I (ANG I).ml-1.h-1]. Neural influences on the kidney were eliminated by renal denervation, and renal perfusion pressure (RPP) was controlled using a clamp on the aorta. Urine flow, sodium excretion, renal blood flow (RBF), glomerular filtration rate (GFR), and cortical and papillary red blood cell (RBC) flow increased significantly after captopril (2 mg/kg iv). Glomerular and peritubular capillary pressures rose by 20%, and vasa recta capillary pressure fell by 3-4 mmHg due to significant reductions in estimated preglomerular, efferent arteriolar and renal capillary-venous vascular resistances. Infusion of ANG II (20 ng.kg-1.min-1 iv) returned RBF, GFR, and glomerular and peritubular capillary pressures to control; however, ANG II did not lower papillary RBC flow before inhibition of prostaglandin synthesis. Saralasin had no effect on papillary RBC flow or the response to captopril. The changes in vasa recta hemodynamics produced by captopril were blocked by a kinin antagonist. These findings indicate that ANG II exerts a vasoconstrictor influence on the renal cortical vasculature of Munich-Wistar rats; however, its effects on the medullary circulation are opposed by vasodilatory eicosanoids. They also suggest that kinins participate in the papillary RBC flow response to captopril, perhaps by reducing the outflow resistance from the vasa recta circulation.