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|All Authors / Contributors:||
Lise Rodat-Despoix; Jean-Pierre Savineau; Université de Bordeaux II,
|Description:||1 v. (187 f.) : ill. en coul. ; 30 cm.|
|Responsibility:||par Madame Lise Rodat-Despoix ; directeur de thèse Jean-Pierre Savineau.|
Chronic hypoxia induces pulmonary arterial hypertension (PAH), which is accompanied by structural and functional changes in pulmonary arteries. Serotonin (5-HT) is one of the key factors responsible for these changes. In this study we show that the reactivity to 5-HT is increased in intrapulmonary arteries (IPA) in rats suffering from PAH induced by a three weeks stay in a hypobaric chamber. In smooth muscle cells (SMC) from IPA, calcium signal induced by 5-HT depends on extracellular Ca2+ and passing through voltage-independent and RHC80267 (1 DAG lipase inhibitor) sensitive channels. This voltage-independent influx is more important in SMC from chronic hypoxic rats than from normoxic rats. The molecular identity of these channels could be linked to the presence of TRPC proteins which are detected in SMC from normoxic and hypoxic rats, as well as in SMC from human pulmonary arteries. Such channels may be considered as a new therapeutic target for PAH, a disease without efficient treatments.