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Basolateral potassium channels of rabbit colon epithelium: role in sodium absorption and chloride secretion

Authors
Journal
Biochimica et Biophysica Acta (BBA) - Biomembranes
0005-2736
Publisher
Elsevier
Publication Date
Volume
1560
Identifiers
DOI: 10.1016/s0005-2736(01)00456-4
Keywords
  • Rabbit Colon Epithelium
  • Basolateral Membrane Potassium Conductance
  • Amphotericin B
  • Quinidine
  • Verapamil
  • 293B

Abstract

Abstract In order to assess the role of different classes of K + channels in recirculation of K + across the basolateral membrane of rabbit distal colon epithelium, the effects of various K + channel inhibitors were tested on the activity of single K + channels from the basolateral membrane, on macroscopic basolateral K + conductance, and on the rate of Na + absorption and Cl − secretion. In single-channel measurements using the lipid bilayer reconstitution system, high-conductance (236 pS), Ca 2+-activated K + (BK Ca) channels were most frequently detected; the second most abundant channel was a low-conductance K + channel (31 pS) that exhibited channel rundown. In addition to Ba 2+ and charybdotoxin (ChTX), the BK Ca channels were inhibited by quinidine, verapamil and tetraethylammonium (TEA), the latter only when present on the side of the channel from which K + flow originates. Macroscopic basolateral K + conductance, determined in amphotericin-permeabilised epithelia, was also markedly reduced by quinidine and verapamil, TEA inhibited only from the lumen side, and serosal ChTX was without effect. The chromanol 293B and the sulphonylurea tolbutamide did not affect BK Ca channels and had no or only a small inhibitory effect on macroscopic basolateral K + conductance. Transepithelial Na + absorption was partly inhibited by Ba 2+, quinidine and verapamil, suggesting that BK Ca channels are involved in basolateral recirculation of K + during Na + absorption in rabbit colon. The BK Ca channel inhibitors TEA and ChTX did not reduce Na + absorption, probably because TEA does not enter intact cells and ChTX is ‘knocked off’ its extracellular binding site by K + outflow from the cell interior. Transepithelial Cl − secretion was inhibited completely by Ba 2+ and 293B, partly by quinidine but not by the other K + channel blockers, indicating that the small (<3 pS) K VLQT1 channels are responsible for basolateral K + exit during Cl − secretion. Hence different types of K + channels mediate basolateral K + exit during transepithelial Na + and Cl − transport.

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