Preeciampsia — A State of Prostaglandin Deficiency? Urinary Prostaglandin Excretion, the Renin-Aldosterone System, and Circulating Catecholamines in Preeciampsia

Urinary excretion of prostaglandin E2 (PGE2) and F ^ (PGF^), plasma concentrations of renin, aldosterone, norepinephrine (NE) and epinephrine (E) were determined during pregnancy, 5 days, 3, and 6 months after delivery in preeciampsia, normotensive pregnant, and nonpregnant control subjects. The PGE2 was higher in normotensive pregnant control subjects than in nonpregnant subjects. In preeciampsia, PGE, was reduced to nonpregnant level. PGF^ was the same in preeciampsia and in normotensive pregnancy, but elevated when compared to the normotensive nonpregnant control group. Plasma concentrations of renin and aldosterone were increased during pregnancy, but considerably less in preeciampsia than during normotensive pregnancy. NE and E were the same as in nonpregnant subjects during both hypertensive and normotensive pregnancy. All parameters were normal 3 months after delivery. There were no correlations between PGE2, PGF^, plasma concentrations of renin, aldosterone, NE, or E and blood pressure level in third trimester either in preeciampsia or in normotensive pregnancy. PGE, was positively correlated to plasma concentrations of renin. It is suggested that the lack of renal PGE2 in preeciampsia might be responsible for the decrease in renal blood flow and sodium excretion. It is hypothesized that preeciampsia is a state of prostaglandin deficiency. The changes in the renin-aldosterone system may be secondary to changes in prostaglandin concentration both in preeciampsia and normotensive pregnancy. (Hypertension 5: 105-111, 1983)