Ole Holger Petersen

Electrogenic Sodium Pump in Pancreatic Acinar Cells

Electrogenic sodium pumps have been described in many excitable tissues, but hitherto not with certainty in epithelial tissues. In the present work it is shown that readmission of potassium to the bathing solution of mouse pancreatic tissue previously deprived of potassium, causes a marked hyperpolarization of the acinar cell membrane. This hyperpolarization is abolished reversibly by strophanthin-G. This indicates the presence of electrogenic sodium pumping in pancreatic acinar cells.

Electrogenic Sodium Pump in Mouse Liver Parenchymal Cells

Readmitting potassium to potassium-deprived mouse liver segments during intracellular microelectrode recording caused an increase in membrane potential and a gradual reduction in amplitude of electrotonic potentials set up by current pulses applied to another liver cell some distance away. Readmitting K in a high concentration (100 mM) caused a transient hyperpolarization followed by depolarization. The transient hyperpolarization was abolished by Strophanthin-G.

Secretory transmembrane potentials in acinar cells from the cat submandibular gland during perfusion with a chloride-free sucrose solution.

SummaryThe cat submandibular gland was perfused with a normal NaCl Locke solution and a chloride-free sucrose solution. The numerical increase in acinar membrane potential (secretory potential) was recorded after intra-arterial injection of acetylcholine.There was no significant difference between the size of the secretory potentials recorded during perfusion with the sucrose solution [23.6 mV±1.4 (n=23)] and the size of those recorded during the control periods [20.6 mV±1.2 (n=24)].The maximal value of the membrane potential after injection of acetylcholine was higher [51.8 mV±2.4 (n=23)] during perfusion with the sucrose solution than during the control periods [44.8 mV±1.8 (n=22)].The results show that a pump transporting chloride into the acinar cells cannot be responsible for the generation of the secretory potentials. The results are best accounted for by assuming that an outward passive transport of potassium, being partly short-circuited by an inward passive sodium transport, is responsible for the change in membrane potential after stimulation with acetylcholine.

Biphasic membrane potential changes in pancreatic acinar cells following short pulses of acetylcholine stimulation.

Acinar cell membrane potentials were measured by intracellular micro-electrode recording from isolated segments of mouse pancreas. At the normal resting potential (r. p.) of -40 mV a short lasting pulse of local acetylcholine stimulation (micro-iontophoresis) evoked a monophasic depolarization. At relatively low r. p. biphasic potential changes (depolarization - hyperpolarization) were observed. Strophanthin-G (1 mM) immediately reduced r. p., but had no effect on the secondary hyperpolarization.