THE RENAL KALLIKREIN‐KININ SYSTEM AND SODIUM EXCRETION

Abstract

Renal kallikrein is a glandular type kallikrien situated in the distal tubular cells and is released into both the urine and the renal lymph. In the vasculature it lowers blood pressure and increases vascular permeability. Blood volume expansion with 0·9% saline or 2·5% glucose leads to a large increase in kallikrein release which, by its effect on the vasculature, helps to maintain dynamic equilibrium. Kallikrein is also released by increase of renal artery pressure or by renal vasodilators. Very small doses of noradrenaline release kallikrein via prostaglandin E as intermediate. Hypertensive doses of angiotensin release kallikrein, partly via prostaglandin and partly by a direct pressure effect. During escape from the sodium‐retaining effect of steroids, kallikrein excretion is increased but it is not released by the acute infusion of aldosterone into the renal artery. The kallikrein‐kinin system antagonizes the renin‐angiotensin system, causes dilution of urine and increases sodium excretion unless renal artery pressure is low. Increased blood pressure can produce natriuresis without involving the kallikrein system, perhaps through release of natriuretic hormone.