Intracellular calcium regulates basolateral potassium channels in a chloride-secreting epithelium

Michael J Welsh; John D McCann

doi:10.1073/pnas.82.24.8823

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Intracellular calcium regulates basolateral potassium channels in a chloride-secreting epithelium

Journal article

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Peer reviewed

Intracellular calcium regulates basolateral potassium channels in a chloride-secreting epithelium

Michael J Welsh and John D McCann

Proceedings of the National Academy of Sciences - PNAS, Vol.82(24), pp.8823-8826

1985

DOI: 10.1073/pnas.82.24.8823

PMID: 2417229

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https://www.ncbi.nlm.nih.gov/pmc/articles/391530View

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Abstract

The two individual cell membranes of epithelia are functionally coupled, so that changes in apical membrane conductance are paralleled by changes in basolateral K+ conductance. However, the signal that regulates basolateral K+ conductance, thereby coupling the two membranes, is unknown. We tested the hypothesis that the cellular calcium concentration, [Ca2+]c, may regulate basolateral K+ conductance in canine tracheal epithelium, a Cl- -secreting epithelium that shows marked membrane coupling. Three findings support the hypothesis. First, the intracellular Ca2+ antagonist 8-(diethylamino)octyl 3,4,5-trimethoxybenzoate hydrochloride (TMB-8) attenuated the secretory response. Second, the secretagogue epinephrine increased [Ca2+]c, as measured with quin-2. Third, we found a K+ channel that was activated by Ca2+ on the cytosolic side of the membrane. Thus, cytosolic Ca2+ regulates the basolateral K+ conductance and may be the signal responsible for functional coupling of the two cell membranes.

Cell Physiology

Fundamental and applied biological sciences. Psychology

Biological and medical sciences

Molecular and cellular biology

Membrane and intracellular transports

Details

Title: Subtitle: Intracellular calcium regulates basolateral potassium channels in a chloride-secreting epithelium
Creators: Michael J Welsh - Univ. Iowa, coll. medicine
John D McCann - Univ. Iowa, coll. medicine
Resource Type: Journal article
Publication Details: Proceedings of the National Academy of Sciences - PNAS, Vol.82(24), pp.8823-8826
DOI: 10.1073/pnas.82.24.8823
PMID: 2417229
NLM abbreviation: Proc Natl Acad Sci U S A
ISSN: 0027-8424
eISSN: 1091-6490
Publisher: National Academy of Sciences; Washington, DC
Language: English
Date published: 1985
Academic Unit: Neurology; Molecular Physiology and Biophysics; Pulmonary, Critical Care, and Occupational Medicine; Fraternal Order of Eagles Diabetes Research Center; Neurosurgery; Internal Medicine
Record Identifier: 9984020859402771

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