Membrane potential, resistance, and intercellular communication in the lacrimal gland: effects of acetylcholine and adrenaline.

Abstract

Intracellular microelectrode recordings were made from surface acini of mouse exorbital lacrimal glands. The impaled cells were stimulated by iontophoresis of acetylcholine (ACh), adrenaline [epinephrine] or isoprenaline from an extracellular micropipette. During exposure to standard Krebs solution the resting membrane potential was -42.5 mV .+-. 1.2 and the resting input resistance 3.3 M.OMEGA. .+-. 0.3. When the tips of the 2 intracellular microelectrodes were more than 100 .mu.m apart no electrical coupling between 2 impaled cells could be detected. At intertip distances below about 80 .mu.m coupling was frequently observed. In all such cases the coupling ratio was 1. The resting current-voltage relation was almost linear within the membrane potential range of -30 to -80 mV. During exposure to standard Krebs solution short iontophoretic pulses of ACh or adrenaline caused fully reversible hyperpolarizations accompanied by marked reduction of surface cell membrane resistance and membrane time constant. The effects of ACh were blocked by atropine (1.4 .times. 10-6 M). Iontophoresis of isoprenaline never had any detectable effect on membrane potential or resistance. Applying de- or hyperpolarizing direct currents through one of the 2 intracellular microelectrodes, the effect of ACh or adrenaline could be observed at different levels of resting potential. Depolarizing the acinar cell membrane resulted in an enhanced stimulant-evoked hyperpolarization whereas hyperpolarizing the acinar cell membrane resulted in a reduction, and at potentials more negative than -60 mV in a reversal of the stimulant-evoked potential change. The ACh equilibrium potential (EACh) under control conditions was -56.6 mV .+-. 1.1 and EAdrenaline was -61.4 mV .+-. 1.0. Replacing the control superfusion solution by a Cl-free sulfate solution resulted in an immediate shift of EACh towards more negative values. At steady state in the Cl-free solution the resting input resistance was 6.8 M.OMEGA. .+-. 1.3. EACh was -95.9 mV .+-. 3.4. Reducing [K]o [outside concentration of potassium] from the usual 4.7 to 1.0 mM resulted in an immediate marked increase in the amplitude of ACh-evoked hyperpolarization whereas increasing [K]o to 10 mM almost abolished the ACh-evoked potential, but not resistance change. Both ACh and adrenaline acted on the lacrimal acinar cell membrane by opening up pathways mainly permeable to K, but also somewhat permeable to Na. This resulted in a release of K and an uptake of Na into the acinar cells.