| Project/Area Number |
04454530
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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 |
Biological pharmacy
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| Research Institution | University of Tokyo |
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Principal Investigator |
NAGAO Taku Univ.of Tokyo, Dept.of Toxicol.& Pharmacol.Professor, 薬学部, 教授 (30217971)
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| Co-Investigator(Kenkyū-buntansha) |
AKAHANE Satomi Univ.of Tokyo, Dept.of Toxicol.& Pharmacol., 薬学部, 助手 (00184185)
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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 |
¥6,700,000 (Direct Cost: ¥6,700,000)
Fiscal Year 1993: ¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 1992: ¥3,900,000 (Direct Cost: ¥3,900,000)
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| Keywords | Ca^<2+>antagonist / Ca^<2+>channel / Ca^<2+> current / diltiazem / nifedipine / verapamil / hypertension / ischemia / 心筋 / パッチクランプ / 高血圧自然発症ラット / 大動脈 |
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| Research Abstract |
An analysis of the mechanism of Ca antagonists was studied in the pathological model condition.
(1) The number of Ca channels in aortas of SHR and WKY rats are not significantly different, even when hypertension is established in SHR.
(2) The effects of diltiazem and its quaternary derivatives on ICa(L) in isolated ventricular myocytes were studied in normal and different pH conditions. We found that diltiazem acts from outside of the membrane.
(3) The effects of elevation of extracellular K+ concentration on the negative inotropic potencies of Ca antagonists were investigated in guinea-pig ventricular muscle. We found that the differential effects of the Ca antagonists are explained by the differences in voltage dependency of their use-dependent blocking effects on ICa(L).
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