Delayed shrinkage triggered by the Na+-K+ pump in terbutaline-stimulated rat alveolar type II cells.
Terbutaline (10 microm) 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.
Hosoi
Keita
K
Department of Physiology, Osaka Medical College, Takatsuki, 569-8686, Japan.
Min
Kyong-Yob
KY
Iwagaki
Akitaka
A
Murao
Hitoshi
H
Hanafusa
Toshiaki
T
Shimamoto
Chikao
C
Katsu
Ken-Ichi
K
Kato
Masumi
M
Fujiwara
Shoko
S
Nakahari
Takashi
T
D000584:Amiloride / Q000031:analogs & derivatives* / Q000494:pharmacology; D000818:Animals; D004791:Enzyme Inhibitors / Q000494:pharmacology; D007476:Ionophores / Q000494:pharmacology; D008297:Male; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000493:pharmacokinetics; D026902:Potassium Channel Blockers / Q000494:pharmacology; D011650:Pulmonary Alveoli / Q000166:cytology / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D012964:Sodium / Q000493:pharmacokinetics; D026941:Sodium Channel Blockers / Q000494:pharmacology; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors / Q000378:metabolism*; D013566:Sympathomimetics / Q000494:pharmacology*; D013726:Terbutaline / Q000494:pharmacology*; D019789:Tetraethylammonium / Q000494:pharmacology; D014634:Valinomycin / Q000494:pharmacology; D014882:Water-Electrolyte Balance / Q000187:drug effects / Q000502:physiology*
D004791:Enzyme Inhibitors; D007476:Ionophores; D026902:Potassium Channel Blockers; D026941:Sodium Channel Blockers; D013566:Sympathomimetics; C013407:benzamil; D014634:Valinomycin; D010042:Ouabain; D019789:Tetraethylammonium; D000584:Amiloride; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D013726:Terbutaline; D011188:Potassium