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Department of Physiology, Department of Internal Medicine (1 First Division2 Second Division) and 3 Central Clinical Laboratory, Osaka Medical College, Takatsuki 569-8686, Japan
Terbutaline (10 µM) induced a triphasic volume change in alveolar type II (AT-II) cells: an initial shrinkage (initial phase) followed by cell swelling (second phase) and a gradual shrinkage (third phase). The present study demonstrated that the initial and the third phases are evoked by the activation of K+ and Cl– channels and the second phase is evoked by the activation of Na+ and Cl– channels. Ouabain blocked the third phase, although it did not block the initial and second phases. This suggests that the third phase is triggered by the Na+–K+ pump. Tetraethylammonium (TEA, a K+ channel blocker) decreased the volume of AT-II cells and enhanced the terbutaline-stimulated third phase, although quinidine, another K+ channel blocker, increased the volume of AT-II cells. The TEA-induced cell shrinkage was inhibited by ouabain, suggesting that TEA increases Na+–K+ pump activity. Ba2+, 2,3-diaminopyridine and a high [K+]o (30 mM) similarly decreased the volume of AT-II cells. These findings suggest that depolarization induced by TEA increases Na+–K+ pump activity, which increases [K+]i. This [K+]i increase, in turn, hyperpolarizes membrane potential. Valinomycin (a K+ ionophore), which induces hyperpolarization, decreased the volume of AT-II cells and enhanced the third phase in these cells. In conclusion, in terbutaline-stimulated AT-II cells, an increase in Na+–K+ pump activity hyperpolarizes the membrane potential and triggers the third phase by switching net ion transport from NaCl entry to KCl release.
(Received 27 September 2003;
accepted after revision 23 March 2004; first published online 1 April 2004)
Corresponding author T. Nakahari: Department of Physiology, Osaka Medical College, Takatsuki, 569-8686, Japan. Email: takan{at}art.osaka-med.ac.jp
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