| Project/Area Number |
06670050
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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 University, School of Medicine, Associate professor, 医学部, 助教授 (50064580)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1995: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1994: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | Ca^<2+> store / chromaffin cells / muscarine / bradykinin / histamine / catecholamine / thapsigargin / ryanodine / カテコルアミン分泌 / 「刺激-分泌」連関 / レセプター刺激 / 細胞内カルシウムストア / マンガン消光法 / サプシガルギン / リアノジン |
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| Research Abstract |
Changes in[Ca^<2+>]i and catecholamine release in rat adrenal chromaffin ells stimulated by muscarine, bradykinin and histamine were analyzed. The continuous receptor stimulation induced a biphasic increase, a prominent initial transient followed by a sustained phase, in either[Ca^<2+>]i or secretion. The initial component of[Ca^<2+>]i change contained a contribution of Ca^<2+> released from intracellular Ca^<2+> stores. This release of Ca^<2+> was completely inhibited by either thapsigargin or ryanodine, suggesting that both inositol trisphosphte-and caffeine-sensitive channels reside on Ca^<2+> stores in rat chromaffin cells. It was found that the inhibition of Ca^<2+> release did not appreciably affect secretory responses evoked by these agonists in a medium containing Ca^<2+> at normal concentrations. Thus, both the initial transient and sustained secretion depend exclusively on Ca^<2+> entry following receptor stimulation. In a medium containing Ca^<2+> at as low concentration as 16 uM,the initial component of bradykinin-evoked secretion was sustained at 59% of that in the normal medium, but was reduced to 23% after inhibition of Ca^<2+> release from stores with thapsigargin. This suggests that Ca^<2+> released from stores mayreinforce the Ca^<2+> entry which is attenuated so much in Ca^<2+>-deficient medium or in some other condition that the Ca^<2+> entry alone can not evoke a robust secretion.
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