The major fluid production in the salivary glands occurs in the acinar cells. In many glands (e.g. the cat submandibular gland used in the present work) there is no secretion during resting conditions. Intraarterial infusion of acetylcholine (ACh) to the gland evokes a vigorous secretion. The immediate action of ACh on the contraluminal acinar cell membrane is to increase the membrane potential. This hyperpolarization is due to a passive outward potassium (K) transport being only partly short-circuited by an inward sodium (Na) transport. Thus the intracellular Na concentration is enhanced by ACh stimulation. Secretion is probably initiated as a consequence of this increased Na concentration either directly activating a sodium chloride (NaCl) pump at the luminal membrane or indirectly activating the secretory mechanism by increasing the calcium influx. In addition to the NaCl pump, which can be inhibited by ethacrynic acid, there is a pump extruding Na and accumulating K, which can be inhibited by g-strophanthin.