Isoproterenol increases Na+-K+-ATPase activity by membrane insertion of α-subunits in lung alveolar cells

American Journal of Physiology - Lung Cellular and Molecular Physiology - Tập 276 Số 1 - Trang L20-L27 - 1999
Alejandro M. Bertorello1, Karen M. Ridge2, Alexander Chibalin1, Adrian I. Katz3, Jacob I. Sznajder2
1Department of Molecular Medicine, Karolinska Institutet, Karolinska Hospital, S-171 76 Stockholm, Sweden;
2Department of Pulmonary and Critical Care Medicine, Michael Reese Hospital, University of Illinois at Chicago, Chicago 60616; and
3Department of Medicine, University of Chicago, Chicago, Illinois, 60637

Tóm tắt

Catecholamines promote lung edema clearance via β-adrenergic-mediated stimulation of active Na+transport across the alveolar epithelium. Because alveolar epithelial type II cell Na+-K+-ATPase contributes to vectorial Na+flux, the present study was designed to investigate whether Na+-K+-ATPase undergoes acute changes in its catalytic activity in response to β-adrenergic-receptor stimulation. Na+-K+-ATPase activity increased threefold in cells incubated with 1 μM isoproterenol for 15 min, which also resulted in a fourfold increase in the cellular levels of cAMP. Forskolin (10 μM) also stimulated Na+-K+-ATPase activity as well as ouabain binding. The increase in Na+-K+-ATPase activity was abolished when cells were coincubated with a cAMP-dependent protein kinase inhibitor. This stimulation, however, was not due to protein kinase-dependent phosphorylation of the Na+-K+-ATPase α-subunit; rather, it was the result of an increased number of α-subunits recruited from the late endosomes into the plasma membrane. The recruitment of α-subunits to the plasma membrane was prevented by stabilizing the cortical actin cytoskeleton with phallacidin or by blocking anterograde transport with brefeldin A but was unaffected by coincubation with amiloride. In conclusion, isoproterenol increases Na+-K+-ATPase activity in alveolar type II epithelial cells by recruiting α-subunits into the plasma membrane from an intracellular compartment in an Na+-independent manner.

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American Journal of Physiology - Lung Cellular and Molecular Physiology

Tập 276 Số 1

L20-L27

Thông tin tác giả