Acute effect of furosemide on renal kallikrein and prostaglandin systems in mild to moderate essential hypertension.

The activity of basal 24-hour urinary kallikrein activity (UKA), prostaglandin E2 (U. PGE2) and thromboxane B2 (U. TxB2) and their relationship to natriuresis (U. Sodium), urinary aldosterone (U. Aldosterone) and plasma renin activity (in supine position: PRA1; in standing position: PRA2) were evaluated in 20 patients with early-moderate hemodynamically defined (first pass and gate blood pool radionuclide angiocardiography) essential hypertension (H) and in 13 age-matched normotensive patients (N). In basal conditions, UKA and PRA2 were significantly reduced (p less than 0.005 and p less than 0.05, respectively) in H compared with N. However, no differences between N and H were found for U. TxB2, U. PGE2, U. Aldosterone, U. Sodium, and PRA1. All parameters were also evaluated both in H and N before and after the administration of furosemide (40 mg i.v.). In H, but not in N, furosemide induced an increase of UKA (p less than 0.05), U. TxB2 (p less than 0.05) and U. Sodium (p less than 0.001). In both H and N furosemide caused a significant rise of PRA1 (p less than 0.001 in H and p less than 0.01 in N) and PRA2 (p less than 0.001 in H and p less than 0.05 in N). In H a significant correlation was found between percent increases of U. Sodium and U. Kallikrein (r = 0.54, p less than 0.01) and between percent differences of PGE2 and TxB2 (r = 0.59, p less than 0.01). It is proposed that reduction of basal UKA may be an early evidence of the first stages of hypertension, i.e., in absence of renal and cardiovascular alteration. The finding is not accompanied by significant changes in urinary excretion of arachidonic acid metabolites and aldosterone. Finally, any relation between UKA values and systemic hemodynamics is lacking.