| Project/Area Number |
06670068
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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 | The Jikei University School of Medicine |
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Principal Investigator |
KURIHARA Satoshi Jikei Univ.School of Medicine, Faculty of Medicine, Professor, 医学部, 教授 (90057026)
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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 |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1995: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1994: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | acidosis / myocardium / intracellular Ca / troponin / intracellular pH / sarcoplasmic reticulum / skinned fiber / aequorin / 細胞内PH / 筋長 / 短縮 |
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| Research Abstract |
Effects of intracellular acidification on Ca^<2+> handling mechanisms and tension development were studied using intact and skinned preparations. CO_2 acidosis (ACD) increased Ca^<2+> transient (CaT) and prolonged its decay time, although tension was inhibited without a significant change of its time course. ACD decreased the Ca sensitivity of the contactile elememts and suppressed the maximal tension in tetanized-preparations. A transient increase in CaT (extra-Ca), which was induced by a quick release of muscle from Lmax to 92% Lmax during a twich contraction, was decreased by ACD.This further suggests a decrease in the Ca sensitivity of the contractile elements. The effects of H^+ on the Ca^<2+> handling of the sarcoplasmic reticulum (SR) weere examined using skinned trabeculae in which Ca^<2+> measured using the fluorescent Ca indicator, fluo-3. Ca-induced Ca release (CICR) and Ca^<2+> uptake by tge SR were all inhibited by H^+. CICR induced by pCa 6 was particularly inhibited by H^+. The increase in CaT in ACD is due to a decrease in the Ca sensitivity and the slow decay of the CaT in acidosis is due to the slow uptake of Ca^<2+> by the SR.
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