| Project/Area Number |
02454116
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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 |
General physiology
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| Research Institution | Nagoya University |
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Principal Investigator |
TOMITA Tadao Nagoya University,Dept of Physiol. Professor, 医学部, 教授 (50078763)
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| Co-Investigator(Kenkyū-buntansha) |
TOKUNO Hiroyuki Nagoya Univ.Dept.Physiol.Res.Ass., 医学部, 助手 (60155520)
TAKAI Akira Nagoya Univ.,Dept. Physiol.Ass. Prof., 医学部, 助教授 (50126869)
中山 晋介 名古屋大学, 医学部, 助手 (30192230)
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| Project Period (FY) |
1990 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥5,400,000 (Direct Cost: ¥5,400,000)
Fiscal Year 1992: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1991: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1990: ¥2,800,000 (Direct Cost: ¥2,800,000)
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| Keywords | Smooth muscle / Intracellular pH / Contraction / Membrane current / Intracellular Ca / Na-H exchange / Na-Ca exchange / Cl-HCO_3 exchange / Cl-HCO_3交換 / カルシウムイオン / パッチクランプ / NaーH交換 / カルシウム電流 / 塩化アンモニウム / ニュ-トラルレッド |
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| Research Abstract |
Effects of changes in intracellular pH (pH_i) were studied in several vascular smooth muscles. pHi was estimated by measuring absorption spectrum of a pH-sensitive dye (Me_2CF) intracellularly loaded and membrane currents were measured with the whole-cell clamp method. pH_i increased from 7.2 to 7.6-7.8 during application of NH_4C1 (20 mM) and transiently decreased to 6.7-6.8 after wash-out. Intracellular alkalinization and acidification were accompanied by a slow contraction and a transient contraction. The former was significantly inhibited by phenoxybenzamine, an a-adrenoceptor blocking agent, suggesting a partial contribution of noradrenaline released from intrinsic nerves. When applied during a maintained muscle tone in excess K^+ medium, NH_4C1 produced relaxation. The contraction observed during intracellular acidification was not affected by verapamil, Ca^<2+> channel blocker, but strongly inhibited by removal of the external Ca^<2+>. This suggests that an increase in intracellular H^+ concentration ([H^+]_i) increases Ca^<2+> influx. It is possible that this is due to a secondary activation of Na-Ca exchange, resulting from an increased intracellular Na^+ concentration through Na-H exchange, activated by an increased [H^+]_i.
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