| Project/Area Number |
06671664
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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 |
Obstetrics and gynecology
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
INOUE Yoshihito KYUSHU UNIV.FACULTY OF MEDICINE,LECTURER, 医学部, 助手 (20260698)
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| Co-Investigator(Kenkyū-buntansha) |
SANO Masatoshi KYUSHU UNIV.FACULTY OF MEDICINE,SENIOR LECTURER, 医学部, 講師 (60206000)
NOZAKI Masahiro KYUSHU UNIV.FACULTY OF MEDICINE,LECTURER, 医学部, 助手 (60228319)
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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: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1994: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | Estradiol / Vascular smooth muscle / Voltage-clamp / Ca channel / G-protein / voltage-clamp法 / エストロゲン / 電位固定法 / Ca2+チャンネル / G蛋白 |
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| Research Abstract |
Effects of estradiol on the electrical and mechanical properties of the rabbit basilar artery were investigated by use of microelectrode, patch-clamp and isometric tension recording methods. Estradiol relaxd arterial tissue pre-contracted by excess high-potassium solution in a concentration dependent manner. In Ca-free solution, histamine and caffeine each produced a phasic contraction, but estradiol did not significantly affect their amplitude. Estradiol did not change the resting membrane potential of the artery whether in the presence or absence of TEA.Action potentials observed in the presence of 10mM TEA were abolished by estradiol.
Estradiol inhibited the voltage-dependent Ba current in a concentration-dependent manner. Estradiol inhibited Ba current observed in the presence of nicardipine more than that in the absence of nicardipine. GTP gamma Sin the pipette enhanced the inhibitory actions of estradiol on the Ba current. On the other hand, with GDP beta Sin the pipette, estradiol failed to inhibit the Ba current. Pertussis toxin in (PTX) the pipette totally prevented the inhibitory action of estradiol on the Ba current. Estradiol had no effect on the outward K currents evoked by a membrane depolarization.
These results strongly suggest that estradiol relaxs arterial tissue by inhibition of voltage-dependent Ca channels and that it inhibits both nicardipine-sensitive and-resistant Ca currents via a PTX-sensitive GTP-binding protein. The main target of estradiol among the arterial Ca channels seems to be the micardipine-resistant Ca channel, rather than the micardipine-sensitive one.
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