AJP - Lung Cellular and Molecular Physiology, Vol 259, Issue 6 459-L467, Copyright © 1990 by American Physiological Society

ARTICLES

Mechanisms of sodium and chloride transport across equine tracheal epithelium

G. J. Tessier, T. R. Traynor, M. S. Kannan and S. M. O'Grady
Department of Veterinary Biology, University of Minnesota, St Paul 55108.

Equine tracheal epithelium, stripped of serosal muscle, mounted in Ussing chambers, and bathed in plasmalike Ringer solution generates a serosa-positive transepithelial potential of 10-22 mV and a short-circuit current (Isc) of 70-200 microA/cm2. Mucosal amiloride (10 microM) causes a 40-60% decrease in Isc and inhibits the net transepithelial Na flux by 95%. Substitution of Cl with gluconate resulted in a 30% decrease in basal Isc. Bicarbonate substitution with 20 mM N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid decreased the Isc by 21%. The Cl-dependent Isc was inhibited by serosal addition of 1 mM amiloride. Bicarbonate replacement or serosal amiloride (1 mM) inhibits the net Cl flux by 72 and 69%, respectively. Bicarbonate replacement significantly reduces the effects of serosal amiloride (1 mM) on Isc, indicating its effect is HCO3 dependent. Addition of 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP; 100 microM) causes a 40% increase in Isc. This effect is inhibited by subsequent addition of 10 microM serosal bumetanide. Bumetanide (10 microM) reduces net Cl secretion following stimulation with 8-BrcAMP (100 microM). Serosal addition of BaCl2 (1 mM) causes a reduction in Isc equal to that following Cl replacement in the presence or absence of 100 microM cAMP. These results suggest that 1) Na absorption depends on amiloride-inhibitable Na channels in the apical membrane, 2) Cl influx across the basolateral membrane occurs by both a Na-H/Cl-HCO3 parallel exchange mechanism under basal conditions and by a bumetanide-sensitive Na-(K?)-Cl cotransport system under cAMP-stimulated conditions, and 3) basal and cAMP-stimulated Cl secretion depends on Ba-sensitive K channels in the basolateral membrane.

This article has been cited by other articles:

				B. R. Grubb, A. J. Pace, E. Lee, B. H. Koller, and R. C. Boucher Alterations in airway ion transport in NKCC1-deficient mice Am J Physiol Cell Physiol, August 1, 2001; 281(2): C615 - C623. [Abstract] [Full Text] [PDF]

				J. Loffing, B. D. Moyer, D. Reynolds, B. E. Shmukler, S. L. Alper, and B. A. Stanton Functional and molecular characterization of an anion exchanger in airway serous epithelial cells Am J Physiol Cell Physiol, October 1, 2000; 279(4): C1016 - C1023. [Abstract] [Full Text] [PDF]

				P. K. Dudeja, N. Hafez, S. Tyagi, C. A. Gailey, M. Toofanfard, W. A. Alrefai, T. M. Nazir, K. Ramaswamy, and F. J. Al-Bazzaz Expression of the Na+/H+ and Cl-/HCO-3 exchanger isoforms in proximal and distal human airways Am J Physiol Lung Cell Mol Physiol, June 1, 1999; 276(6): L971 - L978. [Abstract] [Full Text] [PDF]

				M. C. Lee, C. M. Penland, J. H. Widdicombe, and J. J. Wine Evidence that Calu-3 human airway cells secrete bicarbonate Am J Physiol Lung Cell Mol Physiol, March 1, 1998; 274(3): L450 - L453. [Abstract] [Full Text] [PDF]