Characterization of the Ca²⁺ Response Mediated by Activation of β-Adrenoceptors in Rat Submandibular Ducts

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The Ca²⁺ signaling mediated by activation of β−adrenoceptors was studied in a purified preparation of ducts from rat submandibular glands.At concentrations above 1 nM, isoproterenol(ISO)caused a small but significant increase in cytosolic Ca²⁺ concentration([Ca²⁺]_i).The ISO−induced increase in [Ca²⁺]_i was completely inhibited by the β−adrenoceptor antagonist propranolol but not by the α−adrenoceptor antagonist phentolamine.Forskolin was able to mimic the Ca²⁺ response to ISO.These results suggest that the ISO−induced increase in [Ca²⁺]_i in rat submandibular ducts is mediated by an accumulation of cAMP resulting from activation of β−adrenoceptors.In the absence of extracellular Ca²⁺, ISO or forskolin caused a transient increase in [Ca²⁺]_i, indicating Ca²⁺ mobilization from intracellular Ca²⁺ stores.Further, stimulation with ISO failed to mobilize Ca²⁺ after the depletion of intracellular Ca²⁺ stores by phenylephrine or carbachol, suggesting that the cAMP−mediated increase in [Ca²⁺]_i is due to a Ca²⁺ release from inositol trisphosphate(IP₃)−sensitive Ca²⁺ stores.As ISO did not stimulate a detectable production of IP₃, the cAMP−mediated Ca²⁺ mobilization may be evoked by a mechanism different from activation of phosphoinositide hydrolysis.