α1-Adrenergic regulation of Cl− and Ca2+ movements in rat parotid acinar cells

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Abstract
In rat parotid acinar cells, maximal α1-adrenergic receptor stimulation (10−5 M epinephrine +10−5 M propranolol) leads to a rapid (2+ (∼ 800 nM at peak) which decreases to ∼ 50% of peak Ca2+ by 3–4 min. Similarly, cells preloaded with36Cl− show a rapid (36Cl− which returns to ∼80% of resting values in 3–4 min. Both responses are dependent on epinephrine, with half-maximal effects achieved at 2×10−7 M and 2×10−6 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 ∼2 and 3 min, respectively). Maximal epinephrine-induced Ca2+ and Cl− responses are unaffected by the α2-adrenergic antagonist, yohimbine, are completely blocked by the α1-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 α1-adrenocetor stimulation.