Parotid acinar cells: ionic dependence of acetylcholine-evoked membrane potential changes.
Segments of mouse parotid were placed in a superfusion chamber. Surface acini were impaled by one or two micro-electrodes for measurement of membrane potential and resistance. The acinus under investigation was stimulated by micro-iontophoretic application of acetylcholine (ACh) or adrenaline. Neighbouring acinar cells were electrically coupled. Electrical coupling between acinar cells only occurred within restricted domains probably corresponding to an acinus or a group of acini. Passing direct current through one intracellular electrode, the resting potential of an acinus could be set at desired levels and the dependency of the ACh-evoked potential change on the resting potential investigated. The ACh null potential (initial effect) was about--60 mV. A delayed hyperpolarizing effect of ACh could not be reversed. The initial ACh-evoked potential change was sensitive to alterations in extracellular Na, K and Cl concentration. The delayed ACh-evoked hyperpolarization was blocked by ouabain, exposure to Na-free or K-free solutions. It is concluded that ACh increases mainly K and Na membrane conductance causing K efflux and Na influx with a subsequent Na activation of an electrogenic Na pump.
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D002712:Chlorides / Q000502:physiology; D005260:Female; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D009994:Osmolar Concentration; D010042:Ouabain / Q000494:pharmacology; D010306:Parotid Gland / Q000166:cytology / Q000187:drug effects*; D011188:Potassium / Q000502:physiology; D012964:Sodium / Q000502:physiology
D002712:Chlorides; D010042:Ouabain; D012964:Sodium; D000109:Acetylcholine; D011188:Potassium