Cl- secretagogues increase basolateral K+ conductance of frog corneal epithelium.
The stromal-to-tear transport of Cl- by the corneal epithelium of the frog is increased by pharmacological effectors (secretagogues) that are known to raise the intracellular levels of cyclic AMP or Ca2+. It has been shown in the past that the Cl- secretagogues increase the apical membrane permeability to Cl- and thus facilitate the cell-to-tear flux of the anion. In this report, we combine transepithelial and microelectrode studies to show that three of these secretagogues, epinephrine, the Ca2+ ionophore A23187, and forskolin, also increase the K+ conductance of the basolateral membrane by two- to threefold. The increase in the K+ conductance is not dependent on membrane potential, since this increase occurred equally when the basolateral membrane potential either exceeded 60 mV, as measured with microelectrodes, or was depolarized by voltage clamping after apical permeabilization with amphotericin B. It is proposed that both Cl- and K+ conductances are under the control of intracellular mediators that act independently on each pathway. The increase in basolateral K+ conductance favors the Cl- secretory process.
D000666:Amphotericin B / Q000494:pharmacology; D000818:Animals; D001485:Basement Membrane / Q000378:metabolism; D001692:Biological Transport; D000001:Calcimycin / Q000494:pharmacology; D002712:Chlorides / Q000493:pharmacokinetics*; D005576:Colforsin / Q000494:pharmacology; D003315:Cornea / Q000166:cytology*; D004553:Electric Conductivity; D004837:Epinephrine / Q000494:pharmacology; D004848:Epithelium / Q000187:drug effects / Q000378:metabolism; D008839:Microelectrodes; D011188:Potassium / Q000493:pharmacokinetics*; D011892:Rana catesbeiana; D012016:Reference Values
D002712:Chlorides; D005576:Colforsin; D000001:Calcimycin; D000666:Amphotericin B; D011188:Potassium; D004837:Epinephrine