In rat parotid acinar cells, maximal alpha 1-adrenergic receptor stimulation (10(-5) M epinephrine + 10(-5) M propranolol) leads to a rapid (less than 10 s), 4-5-fold elevation in cytosolic Ca2+ (approximately 800 nM at peak) which decreases to approximately 50% of peak Ca2+ by 3-4 min. Similarly, cells preloaded with 36Cl- show a rapid (less than 10 s) 35-50% loss of 36Cl- which returns to approximately 80% of resting values in 3-4 min. Both responses are dependent on epinephrine, with half-maximal effects achieved at 2 x 10(-7) M and 2 x 10(-6) M agonist for Cl- and Ca2+, respectively. In the presence of low extracellular Ca2+ (i.e. with EGTA), the initial rapid changes in cellular Ca2+ and Cl- are unaltered. However, cellular Ca2+ and Cl- levels return to basal values sooner than when extracellular Ca2+ is present (within approximately 2 and 3 min, respectively). Maximal epinephrine-induced Ca2+ and Cl- responses are unaffected by the alpha 2-adrenergic antagonist, yohimbine, are completely blocked by the alpha 1-adrenergic antagonist, SZL-49, and are similar to ion fluxes induced by maximal muscarinic-cholinergic receptor stimulation (10(-5) M carbachol). The data suggest that a close association exists between mobilization of intracellular Ca2+ and Cl- content in rat parotid acinar cells after alpha 1-adrenoceptor stimulation.