Acetylcholine-stimulated chloride flux in tracheal submucosal gland cells

C. M. Yang, J. M. Farley, T. M. Dwyer

Research output: Contribution to journalJournal Article peer-review

22 Scopus citations


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 ~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.

Original languageEnglish
Pages (from-to)1891-1894
Number of pages4
JournalJournal of Applied Physiology
Issue number4
StatePublished - 1988
Externally publishedYes


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