Effects of furosemide and orthostasis on active and inactive renin in normal and anephric man

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Abstract
Active and inactive (acid-activatable) plasma renin in anephric and in normal persons was investigated. In anephric patients (15) plasma concentration of active and inactive renin was 1.15 .+-. 0.2 and 40.7 .+-. 7.1 .mu.U/ml, respectively; angiotensin II (n = 13) was 14.5 .+-. 1.9 pg/ml. Furosemide (n = 10), 40 mg i.v., and upright posture (n = 8) did not change active or inactive renin in the anephric state. In normal men, furosemide (n = 9) within 15 min increased active renin from 29.9 .+-. 5.8 to 82.4 .+-. 14.8 .mu.U/ml (P < 0.001); inactive renin slightly but not significantly decreased from 136.3 .+-. 29.9 to 121.1 .+-. 19.2 .mu.U/ml; orthostasis (n = 15) within 4 h stimulated active renin (P < 0.001) and slightly raised inactive renin (P < 0.05). Both furosemide and orthostasis increased (P < 0.001, each) the proportion of active renin in normal persons. Studies in 1 patient within 24 h after bilateral nephrectomy indicated the half-life to be 30-60 min for active and 2-4 h for inactive renin. Thus, low levels of active renin and considerable amounts of inactive renin and angiotensin II were detected in anephric patients. About 30% of inactive renin in normal plasma apparently is of extrarenal origin. The stimulation of active renin by furosemide and orthostasis is bound to the presence of the kidney. Both maneuvers may stimulate the conversion of inactive to active renin within the human kidney.