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

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.