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J Appl Physiol 65: 1891-1894, 1988;
8750-7587/88 $5.00
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Journal of Applied Physiology, Vol 65, Issue 4 1891-1894, Copyright © 1988 by American Physiological Society

ARTICLES

Acetylcholine-stimulated chloride flux in tracheal submucosal gland cells

C. M. Yang, J. M. Farley and T. M. Dwyer
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216-4505.

The Cl content of isolated tracheal submucosal gland cells was studied using 36Cl as a tracer. 36Cl uptake reached a steady state within 10 min, yielding an estimate of intracellular Cl concentration of approximately 40 mM. Intracellular Cl fell rapidly when ouabain or furosemide was added, indicating that isolated tracheal submucosal gland cells concentrate Cl above its electrochemical equilibrium concentration. Acetylcholine (ACh) caused a Ca2+-dependent decline in cell Cl, with an effective concentration for a 50% response (EC50) of 62 nM; this loss of cell Cl was blocked by atropine or pirenzepine. The EC50 was 6 nM in cells when 95% of the acetylcholinesterase activity was abolished by diisopropylfluorophosphate (DFP) treatment. ACh continued to cause a decline in cell Cl even after a 7-day course of DFP treatment, which has been shown to abolish ACh-stimulated mucous glycoprotein secretion (23). After the 7-day course of DFP treatment, the EC50 for ACh increased to 77 nM. Thus the Cl economy of the tracheal submucosal gland cell resembles that of cells in epithelia that secrete fluid; in addition, the transmitter-dependent loss of cell Cl is under long-term metabolic control of the cell.


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