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肾脏与股血管敏感性及局部血管紧张素生成的体内比较

In vivo comparison of renal and femoral vascular sensitivity and local angiotensin generation.

作者信息

Li T, Zimmerman B G

机构信息

Department of Pharmacology, University of Minnesota, Minneapolis 55455.

出版信息

Hypertension. 1990 Feb;15(2):204-9. doi: 10.1161/01.hyp.15.2.204.

DOI:10.1161/01.hyp.15.2.204
PMID:2406198
Abstract

Experiments were conducted to compare the relative importance of the local renin-angiotensin systems in the rabbit renal and femoral vascular beds and their functional role in hemodynamic regulation. Angiotensin I (Ang I) (0.15 microgram/kg i.v.) elevated mean arterial blood pressure by 18 +/- 1 mm Hg in the renal experimental group and 19 +/- 1 mm Hg in the femoral experimental group; it decreased renal blood flow by 35 +/- 3% but increased femoral blood flow by 31 +/- 8%. All these effects were blocked by intravenous administration of captopril (2 mg/kg bolus injection plus 1 mg/kg/hr). Captopril also lowered mean arterial pressure by 17 +/- 3 and 16 +/- 2 mm Hg in the renal and femoral experimental groups, respectively, and it increased renal blood flow by 32 +/- 10% but reduced femoral blood flow by 21 +/- 4%. As a result, renal vascular resistance was decreased by 36 +/- 5%, but femoral vascular resistance remained unchanged. After captopril, plasma angiotensin II (Ang II) levels were decreased and Ang I levels increased in the two groups. The renal venous-arterial difference of Ang I was increased by captopril, but the femoral venous-arterial difference of Ang I was not, suggesting greater generation of Ang I in the kidney. In a separate group of bilateral nephrectomized rabbits, plasma Ang II levels as well as mean arterial pressure, femoral blood flow, and femoral vascular resistance were not changed by intravenous administration of captopril.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

进行实验以比较局部肾素 - 血管紧张素系统在兔肾血管床和股血管床中的相对重要性及其在血流动力学调节中的功能作用。在肾实验组中,静脉注射血管紧张素I(Ang I)(0.15微克/千克)使平均动脉血压升高18±1毫米汞柱,在股实验组中升高19±1毫米汞柱;它使肾血流量减少35±3%,但使股血流量增加31±8%。所有这些效应均被静脉注射卡托普利(2毫克/千克推注加1毫克/千克/小时)阻断。卡托普利还分别使肾实验组和股实验组的平均动脉压降低17±3毫米汞柱和16±2毫米汞柱,使肾血流量增加32±10%,但使股血流量减少21±4%。结果,肾血管阻力降低36±5%,但股血管阻力保持不变。注射卡托普利后,两组血浆血管紧张素II(Ang II)水平降低,Ang I水平升高。卡托普利使肾血管中Ang I的动静脉差值增加,但股血管中Ang I的动静脉差值未增加,提示肾脏中Ang I生成更多。在另一组双侧肾切除的兔子中,静脉注射卡托普利后,血浆Ang II水平以及平均动脉压、股血流量和股血管阻力均未改变。(摘要截断于250字)

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