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Endothelin-induced phosphoinositide hydrolysis in the muscular layer of stem villi vessels of human term placenta

Mondon F, Doualla-Bell Kotto Maka F, Sabry S, Ferré F. Endothelin-induced phosphoinositide hydrolysis in the muscular layer of stem villi vessels of human term placenta. Eur J Endocrinol 1995;133:606–12. ISSN 0804–4643

In the present study, we examined the relationship between endothelin receptors and phosphoinositide breakdown in muscle explants of placental stem villi vessels. All peptides examined, i.e. endothelin-1 (ET-1), ET-3, sarafotoxin 6b (S6b) and S6c, were able to induce phosphoinositide hydrolysis in a dosedependent manner; ET-1 was more potent than S6b and ET-3, with corresponding EC₅₀ values of 44 ± 16 pmol/l, 18 ± 13 nmol/l and 33 ± 24 nmol/l, respectively. Sarafotoxin induced only moderate stimulation of inositol phosphate accumulation. Both ET-1- and S6b-induced accumulation of inositol phosphate was almost totally (90%) inhibited by 100 µmol/l BQ 123, while the S6c response was not affected by the ET_A receptor antagonist. In contrast, the ET_B receptor antagonist IRL 1038 inhibited S6c-induced inositol phosphate accumulation by more than 80%, whereas inhibition was only about 30% for ET-1 and S6b stimulations. This indicates that both ET_A and ET_B receptors were coupled to the phospholipase C transducing system in the muscular layer of placental stem villi vessels, and there is evidence that the phosphoinositide hydrolysis response is obtained predominantly via ET_A receptor activation.

F Ferré. U.361 INSERM, Maternité Baudelocque, 123 Bid de Port-Royal, 75014 Paris, France

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