Renal synthesis and urinary excretion of eicosanoids during pregnancy in rats.

Abstract

We tested whether vasodilatory prostaglandins (PGs) mediate the adaptation of the maternal renal circulation to pregnancy by assessing production of PGs by kidney tissues in vitro. We reasoned that if PGs are crucial, then local synthetic rates of these hormones would most likely be increased. Glomeruli harvested from gravid rats of gestational days 6, 12, and 20 did not demonstrate greater basal or stimulated syntheses of PGF2 alpha, PGE2, or 6-keto-PGF1 alpha than those from virgin controls. Production of PGE2 and 6-keto-PGF1 alpha by renal cortical slices obtained from pregnant rats was not greater than that of virgins either. Urine 24-h excretory rates of PGE2 and 6-keto-PGF1 alpha, but not PGF2 alpha, were significantly increased during pregnancy (all P less than 0.05 from prepregnant levels). During midgestation, when urinary excretion of PGE2 and 6-keto-PGF1 alpha was greatest, medullary syntheses of these PGs were found to be comparable between virgin and gravid animals. The present study, which fails to show augmented synthesis of PGs by renal tissues derived from gravid rats, is consistent with our previous investigation in which cyclooxygenase inhibition did not reduce the gestational increase of renal hemodynamics or restore the attenuated renal pressor responsiveness to exogenous angiotensin II. Taken together, we conclude that in rats, PGs most likely do not mediate the alterations in the renal circulation observed during pregnancy.