AJP - Lung Cellular and Molecular Physiology, Vol 268, Issue 4 551-L557, Copyright © 1995 by American Physiological Society
Evidence of Na-K-Cl cotransport in airway smooth muscle
K. J. Rhoden and J. S. Douglas
John B. Pierce Laboratory, New Haven, Connecticut 06519, USA.
The presence of the Na-K-Cl cotransporter in airway smooth muscle was
investigated by measuring 86Rb+ (as a marker for K+) and 36Cl- fluxes in
the guinea pig trachealis. K+ uptake consisted of 1) a bumetanide- and
furosemide-sensitive component, 2) a ouabain-sensitive component, and 3) a
bumetanide- and ouabain-insensitive component. Bumetanide and furosemide
inhibited K+ uptake with IC50s of 0.18 and 5.6 microM, respectively.
Bumetanide-sensitive K+ uptake was reduced by the isosmotic replacement of
extracellular Na+ and Cl- with choline and I-, respectively. Bumetanide
caused a reduction in Cl- uptake, and the ratio of bumetanide-sensitive K+
to Cl-uptake was approximately 1:1.75. Bumetanide caused a decrease in
86Rb+ efflux, suggesting that the Na-K-Cl cotransporter mediates both K+
influx and efflux in airway smooth muscle. Ouabain caused an increase in
bumetanide-sensitive 86Rb+ efflux from the guinea pig trachealis, which was
prevented by exposure to a low-Na+ medium, suggesting that Na-K pump
inhibition stimulates outward Na-K-Cl cotransport as a result of an
increase in intracellular Na+ content.
