Renin increases human amnion cell prostaglandin E2 biosynthesis.

Abstract

Chorionic cells are known to produce several protein hormones; among them is prorenin/renin, whose function is unknown at this time. Amnion is contiguous with chorion and plays a part in the mechanism(s) of parturition through increased prostaglandin (PG) production. The purpose of the present study was to determine whether renin has any action on amnion cell PGE2 biosynthesis. Amnion cells in primary monolayer culture were incubated for 16 h with increasing concentrations of renin. Renin induced a concentration-dependent increase in amnion cell PGE2 production (e.g. in picograms of PGE2 per microgram protein/16 h; mean +/- SEM; n = 4; control, 3.01 +/- 0.15; 0.0001 U/mL renin, 9.66 +/- 2.0; 0.001 U/mL renin, 10.36 +/- 1.91; 0.01 U/mL renin, 10.3 +/- 3.36; 0.1 U/mL renin, 13.82 +/- 2.1). Significant stimulation of amnion cell PGE2 by renin is not observed until 2 h of incubation; stimulation continues a further 6 h, with little change in the following 8 h. We tested the possibility that renin's stimulatory effects were due to angiotensin-I (AI) and angiotensin-II (AII) formation by testing the effects of AI and AII directly and that of renin in the presence of saralasin, a potent antagonist of AII action. Saralasin did not inhibit the effect of renin, nor was AI or AII alone (10(-10)-10(-6) M) stimulatory. Thus, we believe that chorionic renin may have a novel role in the regulation of amnion cell PGE2 production that is independent of angiotensin formation.