These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Basolateral K+ channels in airway epithelia. I. Regulation by Ca2+ and block by charybdotoxin.
    Author: McCann JD, Matsuda J, Garcia M, Kaczorowski G, Welsh MJ.
    Journal: Am J Physiol; 1990 Jun; 258(6 Pt 1):L334-42. PubMed ID: 1694404.
    Abstract:
    In airway epithelia, adenosine 3',5'-cyclic monophosphate (cAMP) stimulates Cl- secretion by activating apical membrane Cl- channels and basolateral membrane K+ channels. Cl- channels are regulated by cAMP-dependent phosphorylation, whereas K+ channels are regulated by the cytosolic Ca2+ concentration, [Ca2+]c. Our recent observation that cAMP increases [Ca2+]c suggested that cAMP might indirectly regulate K+ channels by increasing [Ca2+]c. To study regulation of K+ channels we measured 86Rb efflux, single K+ channels in membrane patches, and [Ca2+]c with the fluorescent indicator fura-2. Isoproterenol and Ca2+ ionophore, A23187, transiently increased [Ca2+]c and transiently stimulated 86Rb efflux. Stimulation of 86Rb efflux resulted from release of intracellular Ca2+ stores. 86Rb efflux was blocked by Ba2+ or charybdotoxin, but not by tetraethylammonium. Charybdotoxin prevented all of the 86Rb efflux that was stimulated by A23187 or by forskolin. Charybdotoxin also blocked the low-conductance inwardly rectifying K+ channel (KCLIC) in membrane patches. These results indicate that the KCLIC channel is responsible for the Ca2(+)-dependent increase in K+ permeability in airway epithelial cells. They also indicate that cAMP-induced release of intracellular Ca2+ is sufficient to activate K+ channels.
    [Abstract] [Full Text] [Related] [New Search]