Captopril increases renin release stimulated by furosemide and hypotension in isolated perfused guinea pig kidneys.

Abstract

To clearly understand the feedback mechanism of renin secretion by intrarenal angiotensin II synthesis, we studied the stimulatory effect of captopril, an angiotensin converting enzyme inhibitor, on renin release from the isolated perfused guinea pig kidneys. Captopril did not affect the basal renin secretion. Captopril increased on a dose dependent basis renin release induced by 0.1 mg/ml furosemide; 5.8 +/- 1.3 ng/ml/hr at 0 mg/ml of captopril vs. 8.8 +/- 1.6 ng/ml/hr at 0.01 mg/ml (p < 0.05) and 11.8 +/- 2.4 ng/ml/hr at 0.1 mg/ml (p < 0.01), 15-20 min after furosemide infusion. After lowering the flow rates from 10 to 5 ml/min, renin secretion was not altered during the first 12 minutes. However, after adding 0.1 mg/ml captopril, renin secretion was enhanced within the following 8 minutes (8.3 +/- 1.5 vs. 3.7 +/- 0.5 ng/ml/hr at the end of low flow rate period, p < 0.01). Lowering the perfusion flow of the guinea pig kidneys decreases the NaCl flux at the macula densa and also seems to have a similar effect to furosemide. Therefore, these effects of captopril suggest that intrarenal angiotensin II production has an important role in the regulation of renin secretion, probably via effects on the macula densa function.