Science Links Japan | [Ca2+]i-Dependent Secretory Responses (Salivary Chromogranin A, Flow and Protein) to .ALPHA. and .BETA.-Adrenergic Stimulation in Isolated and Perfused Rat Submandibular Glands.

[Ca2+]i-Dependent Secretory Responses (Salivary Chromogranin A, Flow and Protein) to .ALPHA. and .BETA.-Adrenergic Stimulation in Isolated and Perfused Rat Submandibular Glands.

Accession number;01A0626981

Title;[Ca2+]i-Dependent Secretory Responses (Salivary Chromogranin A, Flow and Protein) to .ALPHA. and .BETA.-Adrenergic Stimulation in Isolated and Perfused Rat Submandibular Glands.

Author; KANNO T (Yanaihara Inst. Inc., Fujinomiya-shi, Jpn) ASADA N (Hokkaido Univ. Education At Asahikawa, Asahikawa, Jpn) NAGASAWA S (Yanaihara Inst. Inc., Fujinomiya-shi, Jpn) YANAIHARA N (Yanaihara Inst. Inc., Fujinomiya-shi, Jpn)

Journal Title;Biomed Res

Journal Code:Z0236B

ISSN:0388-6107

VOL.22;NO.1;PAGE.33-43(2001)

Figure&Table&Reference;FIG.7, REF.37

Pub. Country;Japan

Language;English

Abstract;Chromogranin A-like immunoreactivity (CgA-like IR) is stored in the exocrine cells in the granular convoluted tubule (GCT) in the rat submandibular gland, and highly concentrated CgA-like IR (approximately 1 mM) is secreted into saliva in response to stimulation with phenylephrine, an .ALPHA.-adrenergic agonist, in the isolated and perfused rat submandibular gland. The stimulation caused immediate and prominent increases in secretory responses (CgA-like IR secretion, flow, and protein secretion). The secretory responses to 3 .MU.M-phenylephrine were scarcely inhibited in a Ca2+-deficient environment, and were almost completely inhibited by 100 .MU.M 2-aminoethoxydiphenyl borate (2-APB), an inhibitory modulator of l, 4, 5 trisphosphate (IP3)-mediated Ca2+ release from intracellular stores. These results are compatible with a view that mobilization of Ca2+ from the IP3-sensitive pool may preferentially be involved in the secretory responses to .ALPHA.-adrenergic agonist. The secretory responses to isoproterenol, .BETA.-adrenergic agonist, remained almost unchanged in the Ca2+-deficient environment, and were markedly delayed by 100 .MU.M 2-APB but were regained gradually after removal of 2APB and the agonist. Mobilization of Ca2+ from the pool may also be involved to facilitate synergistic signallings in the .BETA.-adrenergic responses. (author abst.)

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