The renal kallikrein-kinin system and the regulation of salt and water excretion

Abstract

Sodium excretion is correlated with kallikrein excretion in man, rabbits and rats on a free sodium and water intake, but not on a constant sodium or constant water intake. The correlation also exists during arterial infusion of angiotensin II, substance P and various vasodilators. During sodium depletion, the stimulation of the renin-angiotensin system causes increased drinking in rats and rabbits. The high angiotensin levels would stimulate kallikrein excretion. The excretion of water and dilution of urine are facilitated by the renal kallikrein-kinin system, even when antidiuretic hormone is high. This negative correlation between urinary osmolality and kallikrein excretion exists during arterial infusion of angiotensin or substance P and various vasodilators. During renal artery constriction, the kallikrein release per minute decreases, but over successive 10-minute periods, the kallikrein concentration in urine rises. This rise is correlated with some recovery in the clearance of rho-aminohippurate and inulin. Since kallikrein is released into renal lymph during saline infusion at a rate that correlates with its release into the urine, it is suggested that the renal kallikrein-kinin system protects the renal vasculature against the constricting action of the renin-angiotensin system. The decreased release of kallikrein (via the lymphatics into the circulation) during renal artery constriction, or decreased renal compliance, would potentiate the hypertensive effect of these procedures which cause increased renin release.