Regulation of apical and basolateral K+ conductances in rat colon.
1. Apical administration of an ionophore, nystatin, and basolateral depolarization by K+ were used to investigate the regulation of apical and basolateral electrogenic transport pathways for K+ in the rat proximal and distal colon. 2. Administration of nystatin (100 micrograms ml-1 at the mucosal side), in the presence of Na+ and in the presence of a serosally directed K+ gradient, stimulate a large increase in short-circuit current (ISC) and tissue conductance in both colonic segments. This response was composed of a pump current generated by the Na(+)-K(+)-ATPase and of a current cross a quinine-sensitive basolateral K+ conductance. 3. The pump current, measured as Na(+)-dependent or scilliroside-sensitive current in the absence of a K+ gradient, was significantly greater in the distal than in the proximal colon. The pump current was unaltered by pretreatment of the tissue with forskolin (5 x 10(-6) mol 1(-1)). 4. The current across the basolateral K+ conductance, measured as current in the presence of a serosally directed K+ gradient either in the absence of Na+ or in the presence of scilliroside, was increased by the cholinoreceptor agonist, carbachol (5 x 10(-5) mol 1(-1)), but inhibited by forskolin (5 x 10(-6) mol 1(-1)). 5. Basolateral K+ depolarization induced a negative ISC in both colonic segments, which was inhibited by the K+ channel blocker quinine (10(-3) mol 1(-1)) at the mucosal side), but was resistant to tetraethylammonium (5 x 10(-3) mol 1(-1) at the mucosal side). This K+ current across an apical K+ conductance was stimulated in both colonic segments by carbachol, whereas forskolin had no effect, although control experiments revealed that forskolin was still able to open an apical Cl- conductance under these conditions. 6. These results demonstrate that an increase in intracellular Ca2+ concentration induced by carbachol causes an increase in the basolateral and the apical K+ conductance, thereby inducing K+ secretion in parallel with an indirect support of Cl- secretion due to the hyperpolarization of the cell membrane. In contrast, the dominating effect of an increase in the intracellular cyclic AMP concentration is inhibition of a basolateral K+ conductance; a mechanism which might contribute to the inhibition of K+ absorption.
Schultheiss
G
G
Institut für Veterinär-Physiologie, Justus-Liebig-Universität Geissen, Germany.
Diener
M
M
D000818:Animals; D001693:Biological Transport, Active; D002118:Calcium / Q000378:metabolism / Q000502:physiology; D002217:Carbachol / Q000494:pharmacology; D002462:Cell Membrane / Q000378:metabolism / Q000502:physiology; D002712:Chlorides / Q000378:metabolism / Q000494:pharmacology / Q000502:physiology; D005576:Colforsin / Q000494:pharmacology; D003106:Colon / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D004848:Epithelium / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D005260:Female; D007476:Ionophores / Q000378:metabolism / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009761:Nystatin / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism / Q000494:pharmacology / Q000502:physiology*; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D011803:Quinine / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction / Q000502:physiology; D012964:Sodium / Q000378:metabolism / Q000494:pharmacology / Q000502:physiology; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism
D002712:Chlorides; D007476:Ionophores; D015221:Potassium Channels; D009761:Nystatin; D005576:Colforsin; D002217:Carbachol; D012964:Sodium; D011803:Quinine; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium; D002118:Calcium