title: Active potassium transport across guinea-pig distal colon: action of secretagogues.
abstract: 1. Adrenaline (5 microM) stimulated a K+ secretory current by 2.2 mu equiv h-1 cm-2 in isolated guinea-pig distal colonic epithelium. This secretory activity was inhibited entirely by addition of the loop diuretic bumetanide to the serosal solution. On-going K+ uptake via the absorptive pathway was unaltered by these changes. 2. Prostaglandin E2 (PGE2, 2 microM) stimulated electrogenic K+ secretion and Cl- secretion by 3.0 and 3.6 mu equiv h-1 cm-2, respectively. Serosal addition of bumetanide completely inhibited this K+ secretion but blocked only approximately 70% of Cl- secretion. The bumetanide-insensitive Cl- secretory current was dependent on the presence of Cl- and HCO3- in the bathing solutions. 3. Stimulation of electrogenic K+ secretion by PGE2 occurred with a half-maximal concentration of 4 nM, an affinity approximately 300 times higher than that for stimulation of Cl- secretion by PGE2. 4. Forskolin (10 microM) stimulated Cl- secretion by 4.9 mu equiv h-1 cm-2. The apparent K+ secretory rate was increased by only 1.5 mu equiv h-1 cm-2. A bumetanide-insensitive short-circuit current (ISC) was apparent and of the same size as that stimulated by PGE2. 5. Addition of the Ca2+ ionophore A23187 (10 microM), in the presence of indomethacin (1 microM) to reduce prostaglandin production, inhibited the K+ absorptive pathway by 40% and concurrently stimulated a small rate of electrogenic K+ secretion. 6. Active K+ absorption was inhibited by the addition of ouabain, omeprazole or SCH28080 to the mucosal solution. Both omeprazole and SCH28080 also stimulated a small negative ISC, consistent with electrogenic K+ secretion. 7. Association of K+ absorption, K+ secretion and Cl- secretion is indicated by similarities in transport mechanism and by secretagogue regulation. In particular, maximal rates of K+ secretory current require uptake via apical membrane K+ pumps. Such interrelations support a common cellular locus for these ion transport pathways.
authors.affiliation: Federal Research Centre for Nutrition, Institute of Nutritional Physiology, Eggenstein-Leopoldshafen, Germany.
authors.forename: G
authors.initials: G
authors.lastname: Rechkemmer
authors.forename: R A
authors.initials: RA
authors.lastname: Frizzell
authors.forename: D R
authors.initials: DR
authors.lastname: Halm
mesh_terms: D000251:Adenosine Triphosphatases / Q000037:antagonists & inhibitors; D018663:Adrenergic Agents / Q000494:pharmacology; D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects / Q000502:physiology; D018118:Chloride Channels / Q000187:drug effects / Q000378:metabolism; D003106:Colon / Q000187:drug effects / Q000378:metabolism*; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D015232:Dinoprostone / Q000494:pharmacology; D004594:Electrophysiology; D004837:Epinephrine / Q000494:pharmacology; D006168:Guinea Pigs; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D007413:Intestinal Mucosa / Q000187:drug effects / Q000378:metabolism; D008297:Male; D008954:Models, Biological; D018408:Patch-Clamp Techniques; D011188:Potassium / Q000378:metabolism*; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism
chemical_list: D018663:Adrenergic Agents; D018118:Chloride Channels; D016861:Cyclooxygenase Inhibitors; D015221:Potassium Channels; D000251:Adenosine Triphosphatases; D015232:Dinoprostone; D011188:Potassium; D007213:Indomethacin; D004837:Epinephrine