RELATION BETWEEN URINARY KALLIKREIN AND RENAL FUNCTION, HYPERTENSION, AND EXCRETION OF SODIUM AND WATER IN MAN

Kallikrein excretion was measured by the esterase activity of precipitated urinary proteins. There was a highly significant correlation between sodium excretion and kallikrein excretion in normal subjects. The same was true of patients with essential hypertension adjusting to a low-salt diet. Patients with renal failure had a greatly increased excretion of kallikrein which was related to the sodium excretion per ml. of glomerular filtrate. During the escape from the sodium-retaining effect of fludrocortisone there was a sharp rise in kallikrein excretion. This may be the mechanism by which the " escape " is brought about. A water-load of one litre caused a pronounced rise in kallikrein excretion without a change in sodium excretion. The data show that the kidney has two relatively independent mechanisms related to kallikrein excretion: one in response to a water-load and the other in response to a salt-load. Kallikrein might be the intrarenal hormone released in response to changes in the pressure distal to the afferent arteriole which regulates sodium excretion per nephron.