| Project/Area Number |
04670085
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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 |
Neurophysiology and muscle physiology
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| Research Institution | Fukuoka University |
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Principal Investigator |
INOUE Masumi Fukuoka Univ., School of Medicine, Associate Prof., 医学部, 助教授 (40223276)
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| Co-Investigator(Kenkyū-buntansha) |
IMANAGA Issei Fukuoka Univ., School of Medicine, Professor, 医学部, 教授 (40078613)
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| Project Period (FY) |
1992 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1993: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1992: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | cardiac cell / Ca^<2+> / A channel / Ca^<2+> channel / beta adrenergic stimulation / beta受容体刺激 / A電流 / 一過性外向き電流 / モルモット / 4-aminopyridine / TEA / 不活性化 |
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| Research Abstract |
Under Ca^<2+>-free conditions, transient outward currents (I_o)were elicited by application of a command pulse to membrane potentials more positive than -20 mV in the guinea-pig cardiac cell. This current reached a peak within a few milliseconds of stimulation, then decreased exponertially to a plateau level with a time constant of 35 ms. This value did not depend on the membrane potential between +10 and +70 mV.External Cd^<2+> (0.1mM) mimicked the inhibitory effect of Ca^<2+> on I_o. Addition of D600 (1muM) or quinidine (0.1mM) to the perfusate produced a reversible suppression, and replacement of internal K^+ with tetraethylammonium (TEA) induced a complete inhibition of I_o. The steady-state inactiveation of the transient component of I_o was expressed by a Boltzmann relation with a half-inactivation voltage of -33.5mV and a slope factor of 7.5mV.The transient component was almost was completely inhibited by substitution of 4- aminopyridine, but not TEA, for external cations. The beta adrenergic stimulation little altered an amplitude of the transient component, but increased that of the plateau 2.7 times. We suggest that in guinea-pig cardiac cells, extracellular Ca^<2+> at physiological concentrations is masking the activity of an A-like K^+ channel. This finding raises the possibility that the functional expression of A channels in the gunea-pig heart might be modified during the development.
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