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PC Wong, BG Zimmerman, E Kraft, G Kounenis and P Friedman
The objective of this study was to examine the roles of the blockade of formation of angiotensin II and prostaglandins in the renal vasodilator effect of captopril in conscious salt-replete dogs. Blood pressure was recorded from an indwelling catheter and renal blood flow (RBF) was measured with an electromagnetic flowmeter and an implanted flow probe. Plasma renin activity was measured by radioimmunoassay. The effect of captopril (0.2 mg/kg i.v.) on RBF was compared in dogs given either saralasin (0.5 micrograms/kg min i.a.) or indomethacin (5mg/kg i.v.) with that in dogs given saline vehicle. Control plasma renin activity in these groups of animals before drug treatment ranged from 0.74 to 1.18 ng of angiotensin 1 per ml/hr. Captopril decreased blood pressure from 102 +/- 4 to 92 +/- 4 mm Hg (P less than .01) and increased RBF from 278 +/- 23 to 345 +/- 29 ml/min (25%) (P less than .01) in saline vehicle-treated animals. In the presence of intrarenal infusion of saralasin, captopril did not increase RBF but decreased blood pressure slightly. Captopril still increased RBF by 18% in indomethacin-treated dogs. These results suggest that the renal vasodilator effect of captopril in conscious salt-replete dogs is mainly due to the blockade of angiotensin II formation. Furthermore, the renin-angiotensin system appears to have an influence on renal vascular tone even under these basal conditions.
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