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1. Intracellular recording of membrane potential was made from acinar cells of the isolated mouse parotid gland superfused with physiological salt solutions.

2. The mean acinar resting membrane potential was - 68·5 mV during superfusion with Krebs—Henseleit solution. Shift of the superfusion solution to one containing ACh or adrenaline (10^-5 M) always caused a transient hyperpolarization (about 10-15 mV).

3. The membrane potential was mainly dependent on the extracellular K concentration ([K]_o). Increasing [K]_o tenfold decreased the membrane potential by 50 mV. This depolarization was not mediated by ACh release from depolarized nerve endings, since it was seen in the presence of atropine (1·4 x 10^-6 M) and not caused by the accompanying reduction in [Na]_o to 40 mM caused only a small depolarization (less than 10 mV).

4. When the superfusion solution was shifted, during intracellular recording, from a normal Krebs—Henseleit solution ([K] = 4·7 mM) to a K-free solution, a hyperpolarization of about 8 mV was measured. Reintroduction of the normal K-containing solution after a longer period of K deprivation (30-70 min) resulted in a short-lasting pronounced hyperpolarization (about 20 mV) which could be blocked by Strophanthin-G (10^-3 M).

5. In contrast to previous reports, the present findings indicate that the membrane potential of salivary acinar cells is similar, with respect to magnitude and K-dependence, to that of cells of more thoroughly investigated tissues, such as muscle and nerve, and that the membrane Na—K pump is electrogenic, at least when the cells have been loaded with Na.