Urinary excretion of prostaglandin E2, prostaglandin F2 alpha, and thromboxane B2 in normotensive and hypertensive subjects on varying sodium intakes.

Abstract

A deficiency in renal prostaglandins [PG] has been implicated in the pathogenesis of essential hypertension, particularly low renin hypertension. Previous studies of urinary PG as influenced by Na balance and in esential hypertension have been handicapped by problems with assay methodology, inclusion of male subjects and/or failure to standardize daily fluid consumption. Urinary excretion of PGE2, PGF2.alpha. and thromboxane B2 (TxB2) was compared in black and white normotensive and low-renin and normal-renin hypertensive women during 2 protocols producing Na depletion (10 meq Na diet) and NA loading (200 meq Na diet plus the fluorohydrocortisone [florinef] a synthetic mineralocorticoid). A constant fluid, K and caloric intake was maintained throughout. Changes in plasma renin activity, urinary aldosterone excretion and urinary kallikrein excretion were simultaneously assessed. As Na intake decreased from 120 to 10 meq Na/day, increases in urinary PGF2.alpha. (502 .+-. 60 to 1222 .+-. 176 ng/24 h, P < 0.01) and TxB2 (99 .+-. 33 to 216 .+-. 77 ng/24 h, P < 0.05) excretion were observed in normotensive subjects. These increases were not observed in the hypertensive patients, possibly because less renin stimulation was achieved during the low Na diet. Subnormal PG production may have contributed to the lesser renin stimulation. Urinary PGF2.alpha. excretion in hypertensive patients during Na depletion indicated strong influences of race and renin status; i.e., black and normal-renin hypertensives increased urinary PGF2.alpha. excretion during Na depletion, whereas white and low-renin hypertensives did not. When white hypertensives and normotensive subjects consumed either 120 or 200 meq Na diet, there were no consistent differences in urinary excretion of PGE2, PGF2.alpha. or TxB2. With Na loading, urinary PGE2, PGF2.alpha. and TxB2 excretion did not change; whereas urinary kallikrein excretion increased. Urinary excretion of these prostanoids was independent of mineralocorticoid and kallikrein effects upon the kidney. No evidence was found for a role of renal PGE2, PGF2.alpha. and TxB2 in natriuresis in humans. Urinary excretion of these prostanoids was decreased in hypertensive patients only during Na depletion.