Ca2+, but not Membrane Lipid Hydrolysis, Mediates Human Chorionic Gonadotropin Production by Luteinizing Hormone-Releasing Hormone in Human Term Placenta*

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Abstract
We postulated a role for liqid metabolism and Ca2+ in the LHRH-induced release of hCG by human placentas. Term placental cells in suspension prelabeled with [3H]myoinositol were stimulated without or with increasing concentrations of LHRH in the presence of 10 mM LiCl, and total inositol phosphate (IP) was measured by ion exchange chromatography; a nonsignificant 0.9 .+-. 0.08-fold increase over the control value was observed. In contrast, placental cells stimulated with equimolar concentrations of angiotensin II (AII) induced a 4.6 .+-. 0.9-fold increase in total IP (P < 0.01), while rat pituitary cells showed 1.9 .+-. 0.2- and a 2.4 .+-. 0.07-fold increases in total IP production after stimulation with LHRH or AII, respectively (P < 0.05). These increases were blocked by coincubation with specific LHRH and AII antagonists. When 1 .times. 106 placental cells were incubated with 45Ca2+ without and with increasing doses of LHRH for 0-75 s and then filtered under negative pressure, we observed significant incorporation of 45Ca2+. This influx was linear with incubation time, significantly more pronounced in cells exposed to LHRH than in control cells, and showed a dose-response curve to LHRH that reached maximal influx rates of 3.6 .+-. 0.3 nM/min .cntdot. 1 .times. 106 cells with 10-5 M LHRH. This response was completely blocked by coincubation with 10-5 M LHRH antagonists; cobalt chloride and verapamil reduced it by 60% and 80%, respectively. Compared to placental cells stimulated with LHRH alone, those coincubated with LHRH and specific LHRH or Ca2+ antagonists released from 10-100% less hCG. We conclude that Ca2+ participates in the LHRH action in human placentas, but uncoupled to PI turnover.

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