Estradiol stimulates rat renopapillary prostaglandin E2 (PGE2), but not PGF2 alpha biosynthesis.

Abstract

The effects of estrogen on renal prostaglandin (PG) and renin-angiotensin were investigated in rats in relation to sodium metabolism and blood pressure regulation. Regardless of estrous cycle phase, PGE2 urinary excretion in females was 2-3 times higher than that in males and was associated with higher sodium excretion. A positive correlation was observed between urinary PGE2 and free estradiol concentrations. Reno-papillary PGE2 synthesis in vitro after slice incubation was higher in estrous females than in males. Ovariectomy resulted in a marked decrease in PGE2 renal synthesis and excretion, and estradiol administration (50 micrograms, im) restored these to levels comparable to those in cycling females. This estradiol treatment also was associated with a 3-fold rise in PRA without alteration in blood pressure. In estrogen-primed ovariectomized rats, infusion of the angiotensin antagonist Sar1-Ala8-angiotensin II at a rate of 30 micrograms/microliter X h resulted in a further rise in PRA as well as a significant decrease in renal PGE2 synthesis and excretion toward values observed in the ovariectomized animals. In contrast, renal synthesis and excretion of PGF2 showed no fluctuations during identical variations in estrogenic states. The results suggest that estradiol stimulates renal PGE2, but not PGF2 alpha, synthesis not only via a direct stimulatory action, but also through augmentation of the renin-angiotensin II axis. This increase in vasodilatory PGE2 may function to offset the prohypertensive effects of the estrogen-stimulated renin-angiotensin axis.