Long-term effects of aldosterone on kallikrein, prostaglandin E2 and sodium in rats.

Abstract

To assess the long-term effects of mineralocorticoids on the regulation of the synthesis or release of kallikrein and prostaglandin E2 in the renal kallikrein-kininprostaglandin E system, we studied the effects of chronic infusion of aldosterone (50,ug/kg/day) on urinary excretion of total and active kallikrein, and prostaglandin E2 for 10 days in conscious rats on regular intakes of sodium and on sodium loading with 1% NaCI as a drinking water. Chronic infusion of aldosterone induced a prompt and transient decrease in the ratio of sodium to potassium and a sustained increase in urinary prostaglandin E2 excretion in rats on regular diets, whereas urinary total and active kallikrein excretion did not increase significantly until the 4th day of aldosterone infusion. In rats loaded with sodium, aldosterone did not induce any changes in urinary total and active kallikrein excretion, whereas it induced similar changes in the ratio of sodium to potassium and urinary prostaglandin E2 excretion to those in rats on regular diets. Thus, the present results suggest that aldosterone might stimulate the synthesis or release of renal prostaglandin E2 independent of sodium balance. Furthermore, it is also suggested that aldosterone might stimulate the synthesis or release of kallikrein, at least partly, via the same pathway as sodium loading does. mineralocorticoids ; inactive kallikrein ; trypsin-activated kallikrein ; renal prostaglandin E2 ; sodium balance It system 1977; is generally agreed that the renal kallikrein-kinin-prostaglandin (PG) E is involved in the regulation of electrolytes and water excretion (Dunn Levinsky 1979;Carretero and Scicli 1980). It is well established that