TY - JOUR
T1 - Denopamine stimulates alveolar fluid clearance via cystic fibrosis transmembrane conductance regulator in rat lungs
AU - Gu, Xiu
AU - Wang, Zheng
AU - Xu, Jin
AU - Maeda, Sumiko
AU - Sugita, Makoto
AU - Sagawa, Motoyasu
AU - Toga, Hirohisa
AU - Sakuma, Tsutomu
PY - 2006/9/1
Y1 - 2006/9/1
N2 - Objective: The objective of this study was to test the hypothesis that cystic fibrosis transmembrane conductance regulator (CFTR) plays a role in β1-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 2O 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 CFTRinh-172) inhibited the effect of denopamine, a β1-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 β1-adrenergic antagonist, abolished the effects of denopamine on stimulation of alveolar fluid clearance. Although glibenclamide alone or CFTRinh-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 β1-adrenergic agonist-stimulated alveolar fluid clearance in rat lungs.
AB - Objective: The objective of this study was to test the hypothesis that cystic fibrosis transmembrane conductance regulator (CFTR) plays a role in β1-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 2O 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 CFTRinh-172) inhibited the effect of denopamine, a β1-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 β1-adrenergic antagonist, abolished the effects of denopamine on stimulation of alveolar fluid clearance. Although glibenclamide alone or CFTRinh-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 β1-adrenergic agonist-stimulated alveolar fluid clearance in rat lungs.
KW - Alveolar fluid clearance
KW - Beta-adrenergic agonist
KW - Cystic fibrosis transmembrane conductance regulator
KW - Glibenclamide
KW - Pulmonary oedema
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U2 - 10.1111/j.1440-1843.2006.00898.x
DO - 10.1111/j.1440-1843.2006.00898.x
M3 - Article
C2 - 16916328
AN - SCOPUS:33746927075
VL - 11
SP - 566
EP - 571
JO - Respirology
JF - Respirology
SN - 1323-7799
IS - 5
ER -