title: Acetylcholine-evoked potassium transport in the isolated guinea-pig pancreas.
abstract: In this study, K+ concentration was measured in effluent samples from superfused guinea-pig pancreatic pieces in control conditions and during stimulation with ACh, employing the technique of flame photometry. ACh (10(-7)-10(-5) M) evoked a dose-dependent and sustained increase in K+ concentration in the effluent (K+ release). The removal of Ca2+ from the superfusing medium and the addition of 10(-4) M EGTA caused a significant (P < 0.05) reduction in the ACh-evoked K+ efflux. Replacement of extracellular Cl- in the superfusing physiological salt solution with NO3- abolished the ACh-induced K+ efflux. In contrast, when Cl- was replaced with Br-, ACh still evoked marked K+ release. Pretreatment of pancreatic segments with the loop diuretic furosemide (10(-4) M) resulted in an inhibition of K+ efflux elicited by ACh. Stimulation of pancreatic segments with the Na(+)-K(+)-ATPase inhibitor ouabain (10(-3) M) caused a large efflux of K+. In the continuous presence of ouabain, ACh application elicited no further change in the K+ release. The results indicate that ACh-evoked K+ release from guinea-pig pancreatic segments is sensitive to ouabain, Cl-, furosemide and extracellular Ca2+ and that only the basal efflux is augmented by ouabain. The findings provide further evidence that a diuretic-sensitive coupled Na(+)-K(+)-Cl- cotransport system operates in the guinea-pig pancreas, as it does in other similar transporting epithelia, to bring about K+ mobilization.
authors.affiliation: Department of Physiology, Faculty of Veterinary Sciences, University of Extremadura, Cáceres, Spain.
authors.forename: J A
authors.initials: JA
authors.lastname: Rosado
authors.forename: J
authors.initials: J
authors.lastname: Singh
authors.forename: G M
authors.initials: GM
authors.lastname: Salido
authors.forename: L J
authors.initials: LJ
authors.lastname: Garcia
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D002118:Calcium / Q000502:physiology; D002712:Chlorides / Q000502:physiology; D004232:Diuretics / Q000494:pharmacology; D004558:Electric Stimulation; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005665:Furosemide / Q000494:pharmacology; D006168:Guinea Pigs; D066298:In Vitro Techniques; D010042:Ouabain / Q000494:pharmacology; D010179:Pancreas / Q000187:drug effects / Q000378:metabolism*; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism*; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: D002712:Chlorides; D004232:Diuretics; D004791:Enzyme Inhibitors; D015221:Potassium Channels; D010042:Ouabain; D005665:Furosemide; D000254:Sodium-Potassium-Exchanging ATPase; D000109:Acetylcholine; D002118:Calcium