No abstract

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 microunits 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 microunits/ml (P less than 0.001), while inactive renin slightly but not significantly decreased from 136.3 +/- 29.9 to 121.1 +/- 19.2 microunits/ml; orthostasis (n = 15) within 4 h stimulated active renin (P less than 0.001) and slightly raised inactive renin (P less than 0.05). Both furosemide and orthostasis increased (P less than 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.

Inactive renin in normal human plasma was activated in vitro either by cryoactivation (incubation at 0 degrees C/-5 degrees C up to 3 months) or acid-activation (dialysis to pH 3.0 for 48 h followed by diaylsis to pH 7.5). Plasma-renin-concentration was similar after either activation procedure (96 +/- 50 microU/ml vs 100 +/- 43 microU/ml). There was no further significant acid-activable renin after cryoactivation. These data suggest that conversion of inactive to active renin by optimized procedures is complete. The term "total renin" for activation results under these conditions seems to be valid.

A sensitive and specific radioimmunoassay for the measurement of arg-vasopressin (AVP) in human plasma is described. Recovery of added AVP from plasma was about 65-70%. An acetone extraction step was necessary to prevent unspecific blank effects. Sensitivity of the assay is 0.5 pg AVP/ml plasma. In normally hydrated subjects AVP-concentration ranged from 0.7 pg/ml to 5.8 pg/ml and showed a good correlation with plasma osmolality. In patients with complete diabetes insipidus (D.i.) AVP-values were below the sensitivity limit of the method and they were subnormal when D.i. was incomplete. There was no increase of AVP-concentration during fluid restriction in patients with complete or incomplete D.i. In subjects with psychogenic polydipsia AVP-values were normal and dehydration produced adequate rises of plasma AVP. In patients with SIADH (Schwartz-Bartter-syndrome) AVP-values were greatly enhanced (greater than 10 pg/ml) when correlated to plasma osmolality (less than 170 mosmol/kg H2O).