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Denopamine stimulates alveolar fluid clearance via cystic fibrosis transmembrane conductance regulator in rat lungs
Author(s) -
GU Xiu,
WANG Zheng,
XU Jin,
MAEDA Sumiko,
SUGITA Makoto,
SAGAWA Motoyasu,
TOGA Hirohisa,
SAKUMA Tsutomu
Publication year - 2006
Publication title -
respirology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 85
eISSN - 1440-1843
pISSN - 1323-7799
DOI - 10.1111/j.1440-1843.2006.00898.x
Subject(s) - medicine , cystic fibrosis transmembrane conductance regulator , cystic fibrosis , pathology , transmembrane protein , regulator , receptor , biochemistry , chemistry , gene
Objective: The objective of this study was to test the hypothesis that cystic fibrosis transmembrane conductance regulator (CFTR) plays a role in β 1 ‐adrenergic agonist‐stimulated alveolar fluid clearance. Methods: Isotonic 5% albumin solutions containing different pharmacological agents were instilled into the alveolar spaces of the isolated rat lungs. The lungs were inflated with 100% oxygen at an airway pressure of 7 cm H 2 O and placed in a humidified incubator at 37°C. Alveolar fluid clearance was estimated by the progressive increase in the albumin concentration over 1 h. To test the hypothesis, we determined whether CFTR Cl – channel inhibitors (glibenclamide and CFTR inh ‐172) inhibited the effect of denopamine, a β 1 ‐adrenergic agonist, on stimulation of alveolar fluid clearance in the isolated rat lungs. Results: Denopamine increased alveolar fluid clearance in a dose‐dependent manner. Atenolol, a β 1 ‐adrenergic antagonist, abolished the effects of denopamine on stimulation of alveolar fluid clearance. Although glibenclamide alone or CFTR inh ‐172 alone did not change basal alveolar fluid clearance, these CFTR inhibitors inhibited the effect of denopamine on alveolar fluid clearance. Conclusion: CFTR plays a role in β 1 ‐adrenergic agonist‐stimulated alveolar fluid clearance in rat lungs.