Basolateral K sup + channels in airway epithelia. I. Regulation by Ca sup 2+ and block by charybdotoxin
- Univ. of Iowa, Iowa City (USA)
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.
- OSTI ID:
- 6874817
- Journal Information:
- American Journal of Physiology; (USA), Vol. 258; ISSN 0002-9513
- Country of Publication:
- United States
- Language:
- English
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550201* - Biochemistry- Tracer Techniques