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

A deficiency in renal prostaglandins has been implicated in the pathogenesis of essential hypertension, particularly low renin hypertension. Previous studies of urinary prostaglandins as influenced by sodium balance and in essential hypertension have been handicapped by problems with assay methodology, inclusion of male subjects, and/or failure to standardize daily fluid consumption. We compared urinary excretion of prostaglandin E2 (PGE,), prostaglandin F ^ (PGF^), and thromboxane B2 (TxB2) in black and white normotensive and low-renin and normal-renin hypertensive women during two protocols producing sodium depletion (10 mEq sodium diet) and sodium loading (200 mEq sodium diet plus the fludrohydrocortisone Florinef, a synthetic mineralocorticoid). A constant fluid, potassium, and caloric intake was maintained throughout. Changes in plasma renin activity, urinary aldosterone excretion, and urinary kallikrein excretion were simultaneously assessed. As sodium intake decreased from 120 to 10 mEq sodium/day, increases in urinary PGF^ (502 ± 60 to 1222 ± 176 ng/24 hr, p < 0.01) and TxB; (99 ± 33 to 216 ± 77 ng/24 hr, 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 sodium diet. Alternatively, subnormal prostaglandin production may have contributed to the lesser renin stimulation. Furthermore, urinary PGF, excretion in hypertensive patients during sodium depletion indicated strong influences of race and renin status; namely, black and normal-renin hypertensives increased urinary PGF^ excretion during sodium depletion whereas white and low-renin hypertensives did not. When white hypertensives and normotensive subjects consumed either 120 or 200 mEq sodium diet, there were no consistent differences in urinary excretion of PGE2, PGF^, or TxB2. With sodium loading, urinary PGE,, PGF^, and TxB2 excretion did not change, whereas urinary kallikrein excretion increased. Urinary excretion of these prostanoids was therefore independent of mineralocorticoid and kallikrein effects upon the kidney. Thus, we found no evidence for a role of renal PGE2, PGF^, and TxB2 in natriuresis in humans. Urinary excretion of these prostanoids was decreased in hypertensive patients only during sodium depletion. (Hypertension 4: 735-741, 1982)