Parotid kallikrein secretion in the rat after alterations of electrolyte transport and cAMP activity.

The effects of pharmacologically induced alterations of electrolyte transport and cAMP activity on kallikrein secretion - measured as amidolytic activity - in rat parotid gland were tested in vivo. Changes in transepithelial sodium/potassium transport caused a significant alteration of parotid kallikrein handling. Amidolytic activity was inhibited by sodium channel blockade (via amiloride) and stimulated by an increased sodium influx (via the sodium ionophore monensin). Enhanced intracellular cAMP activity (via dibutyryl cAMP and theophylline) caused a significant increase of ductal kallikrein and potassium secretion. Alterations of intracellular calcium-ion concentration (via A 23187 and verapamil) did not influence parotid kallikrein secretion. Parotid kallikrein secretion seems to be dependent on intracellular sodium and cAMP concentration.