The role of renal kallikrein and prostaglandin in the control of renin release

Abstract

Renal prostaglandins and kallikrein are considered to play an important role in the control of renin release. Recently, we have shown that aprotinin, a kallikrein inhibitor, inhibits the stimulation of plasma renin activity (PRA) by either furosemide or a low sodium diet. However, the mechanisms of action of kallikrein are unknown. Since kallikrein may stimulate bradykinin and prostaglandin production, the present study examines the relationship of renal kallikrein and renal prostaglandins in the control of renin release. Furosemide and a low sodium diet stimulated PRA, urinary kallikrein excretion and urinary prostaglandin E2 excretion. Aprotinin and indomethacin inhibited both furosemide and low sodium diet stimulation of PRA. When maximum doses of both aprotinin and indomethacin were given, PRA was more strongly suppressed than by indomethacin alone. The stimulation of urinary kallikrein excretion by furosemide and by a low sodium diet was not inhibited by indomethacin. These results suggest that both renal kallikrein and prostaglandins play an important role in the control of renin release under sodium depletion. Renal kallikrein may also have a direct action on the kidney to release renin.