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

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  • Nezu Akihiro
    Department of Dental Pharmacology,School of Dentistry,Health Sciences University of Hokkaido,Ishikari--Tobetsu,Hokkaido 061-0293,Japan
  • Tanimura Akihiko
    Department of Dental Pharmacology,School of Dentistry,Health Sciences University of Hokkaido,Ishikari--Tobetsu,Hokkaido 061-0293,Japan
  • Tojyo Yosuke
    Department of Dental Pharmacology,School of Dentistry,Health Sciences University of Hokkaido,Ishikari--Tobetsu,Hokkaido 061-0293,Japan

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  • Characterization of the Ca〔2+〕 Response Mediated by Activation of β-Adrenoceptors in Rat Submandibular Ducts
  • Characterization of the Ca 2 Response Mediated by Activation of ベータ Adrenoceptors in Rat Submandibular Ducts
  • Characterization of the Ca2+ Response Mediated by Activation of β-Adrenoceptors in Rat Submandibular Ducts

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Abstract

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.

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