Characterization of the ca2 + response mediated by activation of beta-adrenoceptors in rat submandibular ducts |
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Authors: | Nezu A Tanimura A Tojyo Y |
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Affiliation: | Department of Dental Pharmacology, School of Dentistry, Health Sciences University of Hokkaido, Ishikari-Tobetsu, Japan. |
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Abstract: | The Ca2+ signaling mediated by activation of beta-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 beta-adrenoceptor antagonist propranolol but not by the alpha-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 beta-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. |
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