ヒスタミンによるβ-エンドルフィン様免疫活性の分泌機序に関する研究
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The effect of histamine on the release of β-endorphin-like immunoreactivity (β-END LI) in rats was studied <I>in vivo</I> and <I>in vivo</I> experiments. Intravenous injection of 100μg/ 100g BW of histamine resulted in a significant increase in the plasma β-END-LI level 5, 15 minutes after the injection. Histamine at concentrations of 10<SUP>-12</SUP> to 10<SUP>-9</SUP>M also caused dose-dependent stimulation of release of 0-END-LI from the dispersed cells of the anterior pituitary of rats. On gel-chromatography, the β-END-LI released by incubating the cells with 10<SUP>-9</SUP>M histamine consisted of two components, which eluted in the same positions as human β-lipotropin and human endorphin, respectively.<BR>Addition of 2mM CoCl<SUB>2</SUB> to the incubation medium inhibited histamine-induced β-END LI release from the cells. Histamine H<SUB>1</SUB> receptor antagonist (10<SUP>-6</SUP>M) inhibited histamine-induced β-END-LI release from the cells. Histamine H<SUB>2</SUB> receptor antagonist (10<SUP>-6</SUP>M), however, did not inhibit histamine-induced β-END-LI release. These results indicate that histamine acts directly on the anterior pituitary cells to stimulate β-END-LI release and that calcium ion is involved in the mechanism of this effect.
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