Dexamethasone Increases .BETA.2-Adrenoceptor-Regulated Phosphatidylcholine Secretion in Rat Alveolar Type II Cells.

  • Isohama Yoichiro
    Department of Pharmacological Sciences, Faculty of Pharmaceutical Sciences, Kumamoto University
  • Kumanda Yukie
    Department of Pharmacological Sciences, Faculty of Pharmaceutical Sciences, Kumamoto University
  • Tanaka Katsuyuki
    Department of Pharmacological Sciences, Faculty of Pharmaceutical Sciences, Kumamoto University
  • Kai Hirofumi
    Department of Pharmacological Sciences, Faculty of Pharmaceutical Sciences, Kumamoto University
  • Takahama Kazuo
    Department of Pharmacological Sciences, Faculty of Pharmaceutical Sciences, Kumamoto University
  • Miyata Takeshi
    Department of Pharmacological Sciences, Faculty of Pharmaceutical Sciences, Kumamoto University

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  • Dexamethasone Increases β2-Adrenoceptor-Regulated Phosphatidylcholine Secretion in Rat Alveolar Type 2 Cells
  • Dexamethasone Increases ベータ2 Adrenocept

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Abstract

Insufficient production of pulmonary surfactant in alveolar type II cells is relevant to many lung diseases. To cure its deficiency, glucocorticoid is commonly used in clinical areas. In the present study, we investigated the effect of dexamethasone on the secretion of phosphatidylcholine, a major phospholipid of pulmonary surfactant, in a primary culture of rat alveolar type II cells. Dexamethasone had no effect on the basal secretion rate of phosphatidylcholine. Dexamethasone augmented both the phosphatidylcholine secretion and the cyclic AMP formation increased by terbutaline. Furthermore, dexamethasone increased the number of β-adrenoceptors and mRNA expression of β2-adrenoceptors in type II cells. These findings indicate that dexamethasone increases pulmonary surfactant secretion through an enhancement of β2-adrenoceptor gene expression.

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