Changes in immunoglobulin A secretion induced by sympathetic and taste stimulation in the rat submandibular gland

Bibliographic Information

Title
Changes in immunoglobulin A secretion induced by sympathetic and taste stimulation in the rat submandibular gland
Other Title
  • ラット顎下腺に対する交感神経刺激および味覚刺激によるSIgA分泌量の変化
Author
中井, 政徳
University
大阪歯科大学
Types of degree
博士(歯学)
Grant ID
乙第1599号
Degree year
2015-06-24

Description

We studied the influence of sympathetic nerve and taste stimulation on salivary immunoglobulin A secretion in the rat submandibular gland. Although the flow of the saliva evoked by β-adrenoceptor stimulation was very small in volume, secretion evoked by both acidity and bitterness stimulation was greater than from sympathetic stimulation. A marked secretion of peroxidase was found evoked by isoprenaline. Similar levels of SIgA secretion were evoked by each stimulus. Amylase secretion was enhanced by isoprenaline, citric acid and quinine stimulation. In particular, citric acid was significantly different compared with isoprenaline. A similar level of SIgA secretion was evoked by each of the stimuli. SIgA secretion evoked by both isoprenaline and quinine was significantly inhibited by propranolol. Propranolol had only a slight inhibitory effect on citric acid stimulation. The peroxidase level in response to isoprenaline was remarkably reduced by propranolol administration. Although propranolol was less effective on peroxidase secretion evoked by citric acid, quinineinduced peroxidase stimulation was inhibited by propranolol. However, the amylase activity evoked by acidity was weaker than that of sympathetic stimulated saliva. This differencewas attributable to the influence of the nervous system on IgA secretion through input to the submandibular gland via not only the sympathetic nerves, but also the parasympathetic nerves. These results indicate that the salivary secretion of SIgA is regulated by nerve impulses and that acidity imparts a greater effect on SIgA secretion than does solitary sympathetic stimulation alone.

2015

収集根拠 : 博士論文(送信)
資料形態 : テキストデータ
コレクション : 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文
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収集根拠 : 博士論文(自動収集)
資料形態 : テキストデータ
コレクション : 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文
We studied the influence of sympathetic nerve and taste stimulation on salivary immunoglobulin A secretion in the rat submandibular gland. Although the flow of the saliva evoked by β-adrenoceptor stimulation was very small in volume, secretion evoked by both acidity and bitterness stimulation was greater than from sympathetic stimulation. A marked secretion of peroxidase was found evoked by isoprenaline. Similar levels of SIgA secretion were evoked by each stimulus. Amylase secretion was enhanced by isoprenaline, citric acid and quinine stimulation. In particular, citric acid was significantly different compared with isoprenaline. A similar level of SIgA secretion was evoked by each of the stimuli. SIgA secretion evoked by both isoprenaline and quinine was significantly inhibited by propranolol. Propranolol had only a slight inhibitory effect on citric acid stimulation. The peroxidase level in response to isoprenaline was remarkably reduced by propranolol administration. Although propranolol was less effective on peroxidase secretion evoked by citric acid, quinineinduced peroxidase stimulation was inhibited by propranolol. However, the amylase activity evoked by acidity was weaker than that of sympathetic stimulated saliva. This differencewas attributable to the influence of the nervous system on IgA secretion through input to the submandibular gland via not only the sympathetic nerves, but also the parasympathetic nerves. These results indicate that the salivary secretion of SIgA is regulated by nerve impulses and that acidity imparts a greater effect on SIgA secretion than does solitary sympathetic stimulation alone.
2015

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