| Project/Area Number |
02670036
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
General physiology
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| Research Institution | Niigata University |
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Principal Investigator |
WARASHINA Akira Niigata Univ., Sch. of Med., Dept. of Physiol. Associate professor, 医学部, 助教授 (50064580)
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| Co-Investigator(Kenkyū-buntansha) |
HIRANO Tetsuo Niigata Univ., Sch. of Med., Dept. of Physiol. Associate professor, 医学部, 講師 (50092721)
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| Project Period (FY) |
1990 – 1991
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1991: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1990: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | rat adrenal medulla / catecholamine secretion / intracellular Ca^<2+> store / intracellular free Ca^<2+> / phorbol ester / protein kinase C / muscarine / bradykinin / 細胞内カルシウムストア / ヒスタミン / カルシウム感受性色素(fluoー3) |
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| Research Abstract |
1. Changes in free intracellular Ca2+ concentration, (Ca2+)i, and catecholamine secretion (CA) in muscarine-, bradykinin- and histamine-stimulated medullary cells of the perfused rat adrenal gland were studied by means of microfluorometry with intracellularly loaded Ca2+ indicator dye (fluo-3) and real-time electrochemical detection of catecholamine in the perfusate. The suggested modes of Ca2+ mobilization and its modulation by protein kinase C are as follows :
(1) Rise in (Ca2+)i during continuous stimulation of these receptors occurred in two phases ; transient, initial peak followed by sustained elevation. The CA secretion evoked by these stimulations showed the time-course similar to that of the (Ca2+)i rise.
(2) The initial phase of response was considered to be produced mainly with Ca2+ released from intracellular stores since it was resistive against lowering the extracellular Ca2+ concentration and inhibited by a intracellular Ca2+ antagonist, TMB-8.
(3) The sustained phase of response was mediated by Ca2+ entry associated with receptor activation. This Ca2+ entry was not inhibited by L-type Ca2+ channel blocker, nifedipine.
(4) On treating medullary cells with phorbol esters, the secretory responses by these agonists were modified each in different fashions. The result suggests that the activation of protein kinase C modulates differentially the function of these receptors or/and coupled G-proteins.
2. Rat adrenal medullary cells were isolated by collagenase treatment. Most cells showed large, spontaneous oscillation of (Ca2+)i that occurred in absence of any stimulants and was inhibited in presence of TMB-8. The oscillatory release and uptake of Ca2+ by intracellular Ca2+ stores may be responsible for the phenomenon.
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