The involvement of basolateral potassium channels in the intestinal response to secretagogues in the rat.
The possible involvement of basolateral K+ channels in the intestinal response to secretagogues was investigated using stripped sheets of rat mid-intestine. Increasing the serosal K+ concentration reduced the rise in short-circuit current induced by acetylcholine, 5-hydroxytryptamine, theophylline and prostaglandin E2 (PGE2) without affecting the change caused by glucose. The secretagogue-induced rise in short-circuit current was inhibited by quinine, but not by tetraethylammonium chloride, apamin or 3,4-diaminopyridine. Acetylcholine stimulated 86Rb efflux into the serosal fluid from pre-loaded intestinal sheets and a smaller response was observed with PGE2. The acetylcholine-induced stimulation of 86Rb efflux was inhibited by serosal quinine and lack of serosal Ca2+. Furosemide in the serosal fluid reduced the electrical response to acetylcholine without affecting the increase in 86Rb efflux. It is concluded that as well as increasing luminal Cl- permeability, intestinal secretagogues also enhance the basolateral K+ conductance by activating Ca2+-dependent K+ channels.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000494:pharmacology; D015232:Dinoprostone; D004848:Epithelium / Q000502:physiology; D005947:Glucose / Q000494:pharmacology; D066298:In Vitro Techniques; D007422:Intestines / Q000502:physiology*; D007473:Ion Channels / Q000187:drug effects*; D008297:Male; D011188:Potassium / Q000502:physiology*; D011458:Prostaglandins E / Q000494:pharmacology; D011803:Quinine / Q000494:pharmacology; D051381:Rats; D012413:Rubidium / Q000378:metabolism; D012701:Serotonin / Q000494:pharmacology; D013806:Theophylline / Q000494:pharmacology
D007473:Ion Channels; D011458:Prostaglandins E; D012701:Serotonin; D011803:Quinine; D013806:Theophylline; D005947:Glucose; D015232:Dinoprostone; D012413:Rubidium; D000109:Acetylcholine; D011188:Potassium; D002118:Calcium