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

. We investigated active and inactive (acid-activatable) plasma renin in anephric and in normal persons. In anephric patients (n= 15) plasma concentration of active and inactive renin was 1.15 ± 0.2 and 40.7 ± 7.1 μU/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 (μ/ml (P lt; 0.001), while inactive renin slightly but not significantly decreased from 136.3 ± 29.9 to 121.1 ± 19.2 μU/ml; orthostasis (n= 15) within 4 h stimulated active renin (P < 0.001) and slightly raised inactive renin (P < 005). Both furosemide and orthostasis increased (P < 0.001, each) the proportion of active renin in normal persons. Studies in one patient within 24 h after bilateral nephrectomy indicated half-life to be 30–60 min for active and 2–4 h for inactive renin. Thus, we detected low levels of active renin and considerable amounts of inactive renin and angiotensin II in anephric patients. Our data suggest that about 30%, of inactive renin in normal plasma is of extrarenal origin. The stimulation of active renin by furosemide and orthostasis is bound to the presence of the kidney. Our studies provide indirect evidence that both manoeuvres may stimulate the conversion of inactive to active renin within the human kidney.