1989 Fiscal Year Final Research Report Summary
Calcium channel alterations coupled with secretory response in rat parotid gland cells
| Project/Area Number |
62480379
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Functional basic dentistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
ISHIDA Hajime The Univ. of Tokushima Sch. of Dentistry; Professor, 歯学部, 教授 (70028364)
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| Co-Investigator(Kenkyū-buntansha) |
WATANABE Shinji The Univ. of Tokushima Sch. of Dentistry; Research Associate, 歯学部, 助手 (00201187)
KODA Naohiko The Univ. of Tokushima Sch. of Dentistry; Research Associate, 歯学部, 助手 (60144995)
ISHIKAWA Yasuko The Univ. of Tokushima Sch. of Dentistry; Assistant Professor, 歯学部, 講師 (40144985)
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| Project Period (FY) |
1987 – 1989
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| Keywords | Salivary Glands / Amylase Secretion / Calcium Channel / Calcium Antagonists / Drug Receptors / Phosphatidylinositol / Inositol 1, 4, 5-Triphosphate / [^3H] Nitrendipine |
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| Research Abstract |
It is well known that calcium ion plays an important for role in the regulation of the physiological function of cells. In salivary glands, calcium ion activates the intracellular processes and causes the secretory response. Calcium channel is considered to be very important to regulate the intracellular calcium concentration. We have studied characteristics of the calcium channel in rat parotid ,land cell in relation to secretory response.
Amylase was secreted from rat parotid gland cells by the incubation oil them in the medium containing a calcium ionophore, A23187, or in the medium containing high concentration of K^+. The stimulation by isoproterenol of beta-adrenoceptors or acetylcholine of muscarinic receptors of rat parotid gland cells caused also amylase secretion from the cells. The presence of an adequate concentration of extracellular calcium was necessary for the amylase secretion from rat parotid gland cells. Release of amylase from secretory granules, zymogen granules, in
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rat parotid gland cells was also regulated by a low concentration of calcium. The contents of inositol 1, 4, 5-triphosphate in rat parotid gland dispersed cells were increased about 80% by the incubation of them in the presence of acetylcholine for 5 min. at 37ﾟC. These results showed that calcium ion liberated from an intracellular store of parotid gland cells has a stimulatory effect on amylase secretion. Amylase secretion from rat parotid gland cells caused by acetylcholine or isoproterenoll was not blocked by nifedipine, nicardipine, verapamil, or diltiazem. Binding experiments of [^3H]nitrendipine with rat parotid gland cell membrane did not show the presence of specific binding sites.
These results clarify that the increases in the intracellular concentration of calcium ion entered into rat parotid gland cells through the calcium channel activated by drug receptors and liberated from an intracellular store in the cells by inositol 1, 4, 5-triphosphate play an important role in amylase secretion from the cells. Less
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