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In Vivo Comparison of Renal and Femoral Vascular Sensitivity and Local Angiotensin Generation

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 /ig/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. These results indicate that in the rabbit femoral vascular resistance is not controlled by the renin-angiotensin system directly, and the local renin-angiotensin system in the kidney is more important in regulating renal vascular tone.