This Article Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by BELISLE, S. Articles by GALLO-PAYET, N. Search for Related Content PubMed PubMed Citation Articles by BELISLE, S. Articles by GALLO-PAYET, N.

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

Department of Obstetrics-Gynecology Quebec, Canada J1H5N4
Department of Medecine, University of Sherbrooke Sherbrooke, Quebec, Canada J1H5N4
Department of Pharmacology, University of Sherbrooke Sherbrooke, Quebec, Canada J1H5N4
Department of Biochemistry, University of Sherbrooke Sherbrooke, Quebec, Canada J1H5N4
Department of Faculty of Medecine, University of Sherbrooke Sherbrooke, Quebec, Canada J1H5N4

Address requests for reprints to: Dr. Serge Bélisle, Department of Obstetrics and Gynecology, Faculty of Medicine, University of Sherbrooke, Sherbrooke, Quebec, Canada JlH 5N4.

We postulated a role for lipid 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 (All) 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 All, respectively (P < 0.05). These increases were blocked by coincubation with specific LHRH and All antagonists. When 1 x 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.1 x 10⁶ cells with 10^–6 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 107–100% less hCG. We conclude that Ca²⁺ participates in the LHRH action in human placentas, but uncoupled to PI turnover.

^* This work was supported by a grant from the Medical Research Council of Canada.

Received December 29, 1988.

This article has been cited by other articles:

				K. W. Cheng, P. S. Nathwani, and P. C. K. Leung Regulation of Human Gonadotropin-Releasing Hormone Receptor Gene Expression in Placental Cells Endocrinology, July 1, 2000; 141(7): 2340 - 2349. [Abstract] [Full Text] [PDF]