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Am J Physiol Cell Physiol 269: C267-C274, 1995;
0363-6143/95 $5.00
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AJP - Cell Physiology, Vol 269, Issue 1 C267-C274, Copyright © 1995 by American Physiological Society

ARTICLES

Functional coupling of Na(+)-K(+)-2Cl- cotransport and Ca(2+)-dependent K+ channels in vascular endothelial cells

W. C. O'Neill and D. F. Steinberg
Department of Medicine, Emory University School of Medicine, Atlanta, Georgia 30322, USA.

To determine whether the activation of Na(+)-K(+)-2Cl- cotransport by Ca(2+)-mobilizing agonists is a direct effect of Ca2+ or is secondary to activation of Ca(2+)-dependent K+ channels [via cell shrinkage or decreased intracellular Cl- concentration ([Cl-]), we measured K+ fluxes in aortic endothelial cells in response to ATP and bradykinin. With either agonist there was an immediate bumetanide-insensitive efflux inhibitable by the K+ channel blockers tetrabutylammonium (TBA, 23 mM) and quinidine (1 mM), followed several minutes later by increased bumetanide-sensitive efflux or influx (Na(+)-K(+)-2Cl- cotransport). ATP induced a loss of cell K+ that was prevented by TBA and augmented by bumetanide. Both TBA and quinidine prevented the stimulation of cotransport by agonists but not by hypertonic shrinkage. Raising medium [K+] to prevent K+ loss also blocked activation of cotransport by agonists. The results indicate that the stimulation of Na(+)-K(+)-2Cl- cotransport by Ca2+ is not direct but instead is indirect via activation of Ca(2+)-dependent K+ channels and a resulting decrease in cell volume and intracellular [Cl-]. This suggests that at least one role of Na(+)-K(+)-2Cl- cotransport in endothelial cells is to maintain cell volume and intracellular [Cl-] during agonist stimulation.


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