[Recent advances in the clinical study of the renin system. Reference values and conditions of validity].

Plasma renin activity, angiotensinogen, active renin and aldosterone concentrations and, 1 hour after addition of trypsin 1 mg per ml of plasma at -4 degrees C, prorenin and total renin concentrations were measured in 49 normotensive volunteers. Renin activity and active renin concentration were correlated (n = 98, r = 0.902, p less than 0.01) and their ratio was not dependent on the angiotensinogen concentration. Prorenin accounted for 90 per cent of total renin and was 40 per cent higher in males than in females in both supine and upright positions (p = 0.02 and p = 0.01). The change in position markedly increased plasma renin activity as well as active renin and aldosterone concentrations and, to a lesser degree, prorenin concentration, thereby raising the active/total renin ratio. Plasma renin activity, active renin concentration and plasma aldosterone concentration were significantly and negatively correlated with age, but not with urinary sodium excretion. Plasma renin activity and active renin and angiotensinogen concentrations were also measured in 14 patients with high angiotensinogen concentration (pregnant women and oestrogen users) and in 14 patients with cirrhosis and subnormal angiotensinogen concentration. In these patients the ratio of plasma renin activity to active renin concentration was correlated with the angiotensinogen concentration (n = 28, r = 0.643, p less than 0.01). The slope of the regression line between renin activity and active renin concentration was significantly different in patients with cirrhosis and in healthy volunteers, the measurement of renin activity leading to a ten-fold underestimation of active renin concentration. In clinical investigations of the renin system, plasma samples should be handled at room temperature to avoid cryoactivation of prorenin. The determination of active renin concentration should be preferred to that of plasma renin activity because it is not influenced by physiological or pathological variations in angiotensinogen.