Sodium-independent modulation of na+-k+-atpase activity by [beta]
-adrenergic agonist in alveolar type ii cells.
Suzuki, Satoshi, Danny Zuege, and Yves Berthiaume.
Centre de Recherche H[circumflex]otel-Dieu de Montr[acute]eal and
D[acute]epartement de M[acute]edecine, Universit[acute]e de
Montr[acute]eal, Montreal, Quebec, Canada
APStracts 2:0031L, 1995.
Although [beta]-adrenergic agonists are known to stimulate sodium
transport in alveolar epithelial cells, the exact cellular mechanism
involved in this process is unknown. We determined if terbutaline, a
[beta]-adrenergic agonist, modulated Na+-K+-ATPase in cultured rat
alveolar type II cells by measuring the enzyme's activity via an
adapted radiometric method. The assay conditions were optimized by
evaluating permeabilization techniques and substrate concentrations
for Na+-K+-ATPase measurement at Vmax. Terbutaline at 10-2 M
increased enzyme activity with a maximal response at 15 min that was
completely inhibited by 10-2 M propranolol. This effect of
terbutaline was dependent on the presence of serum as well as on the
time the cells were in culture. The enhancement of Na+-K+-ATPase
activity was reproduced by 10-3 M dibutyryl cyclic AMP and 5 x 10-5 M
forskolin. Neither 10-4 M amiloride nor a sodium-free solution
influenced the effect of terbutaline. Western blotting showed that
terbutaline did not change the expression of the [alpha]1 subunit of
the enzyme, which is the predominant form in this cell type. We
conclude that [beta]-adrenergic agonists can modulate Na+-K+-ATPase
activity partially through cyclic AMP and this process is not
secondary to an increase in intracellular sodium concentration.
Received 12 May 1994; accepted in final form 6 February 1995.
APS Manuscript Number L134-4.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 10 March 1995.