Urinary Prostaglandin E2 and Kallikrein Excretion in Glucocrticoid Hypertension in Rats

Abstract

1. Oral administration of dexamethasone (about 2.5 × 10-⁷ mol/day) caused hypertension in rats. The blood pressure rose from 108 ± 6 (mean ± sd) to 156 ± 17 mmHg on the seventh day. The urine volume and urinary excretion of sodium were increased. The plasma renin activity and plasma aldosterone were unchanged. However, the urinary excretions of prostaglandin E₂ (U_PGE2V) and kallikrein (U_kall.V) were markedly decreased throughout the experiment. 2. With concurrent administration of captopril, the elevation of blood pressure was partially prevented. in this group of rats, the plasma renin activity was elevated and the reductions in U_PGE2V and U_kall.V were partially prevented. 3. Based on these results, it is suggested that suppression of the kallikrein—kinin and prostaglandin systems, in addition to involvement of the renin-angiotensin system, is one of the factors contributing to the hypertensive action of dexamethasone.