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This Article Full Text Full Text (PDF) All Versions of this Article: 561/2/449    most recent jphysiol.2004.073023v1 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 Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Niger, C Articles by Cronier, L Search for Related Content PubMed PubMed Citation Articles by Niger, C Articles by Cronier, L

¹ CNRS UMR 6187, Institut de Physiologie et Biologie Cellulaires, Université de Poitiers, 40, Avenue du Recteur Pineau, 86022 Poitiers Cedex, France
² INSERM U427, Développement, humain et différenciation, Faculté de pharmacie, 75270 Paris cedex 6, France

Ca²⁺ transfer across the syncytiotrophoblast (ST) of the human placenta is essential for normal fetal development. However, the nature of Ca²⁺ conductance in the ST and the mechanisms by which it is regulated are poorly understood. With the major signal transduction pathway of endothelin-1 (ET1) acting via phospholipase C (PLC) and Ca²⁺, we used ET1 to analyse the nature of Ca²⁺ channels on cultured trophoblastic cells by means of cytofluorimetric analysis using the ratiometric Ca²⁺ indicator Indo-1. Results indicate that ET1 (10^–7 M) stimulates a biphasic (transient and sustained) increase in [Ca²⁺]_i in trophoblastic cells. This response is mediated by the endothelin receptor B (ETB) coupled to PLC, since treatment with BQ788 (10^–6 M) or U73122 (2 µM) totally abolished the response. Persistence of the rapid transient rise in [Ca²⁺]_i in Ca²⁺-free extracellular medium confirms the release of Ca²⁺ from intracellular stores in response to ET1 stimulation. Furthermore, abolition of the sustained increase in [Ca²⁺]_i in Ca²⁺-free extracellular medium argues in favour of the entry of Ca²⁺ during the plateau phase. Abolition of this plateau phase by Ni²⁺ (1 mM) in the presence of extracellular Ca²⁺ confirmed the existence of an ET1-induced Ca²⁺ entry. No evidence for the presence of voltage-operated channels was demonstrated during ET1 action since nifedipine (10^–6 M) did not reduce the Ca²⁺ response and depolarization with a hyper-potassium solution had no effect. Pharmacological studies using the imidazole derivatives SK&F96365 (30 µM) and LOE 908 (10 µM) partially inhibited the ET1-evoked Ca²⁺ response, thus providing evidence for the presence of both store-operated Ca²⁺ channels and non-selective cationic channels in the human ST.

(Received 30 July 2004; accepted after revision 1 September 2004; first published online 9 September 2004)
Corresponding author L. Cronier: CNRS UMR 6187, Institut de Physiologie et Biologie Cellulaires, 40 Avenue du Recteur Pineau, 86022 Poitiers Cedex, France. Email: laurent.cronier{at}univ-poitiers.fr

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