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Renin Increases Human Amnion Cell Prostaglandin E₂ Biosynthesis^*

Division of Reproductive Sciences, Department of Obstetrics and Gynecology, University of Utah Medical Center Salt Lake City, Utah 84132

Address requests for reprints to: Dr. Sarah Lundin-Schiller, Department of Obstetrics and Gynecology, Room 2B302, University of Utah Medical Center, 50 North Medical Drive, Salt Lake City, Utah 84132.

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 µg 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 (All) formation by testing the effects of AI and All directly and that of renin in the presence of saralasin, a potent antagonist of All action. Saralasin did not inhibit the effect of renin, nor was AI or All 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.

^* This work was supported in part by NIH Grant HD-20779.

Received October 15, 1990.

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