| Project/Area Number |
10671459
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Urology
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| Research Institution | UNIVERSITY of TOKYO |
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Principal Investigator |
MORIYAMA Nobuo (1999) The Univ. Tokyo, Assist. Prof., 医学部・附属病院, 講師 (80143501)
黒岡 雄二 (1998) 東京大学, 医学部附属病院, 助手 (80161777)
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| Co-Investigator(Kenkyū-buntansha) |
森山 信男 東京大学, 医学部・附属病院, 講師 (80143501)
亀山 周二 東京大学, 医学部・附属病院, 講師 (90186015)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1999: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1998: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | Human renal artery / αィイD21ィエD2-adrenoceptor / αィイD21ィエD2-adrenoceptor mRNA / in situ hybridization / RNAase protection assay / ヒト腎実質 |
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| Research Abstract |
This study was intended to quantify the amounts of the αィイD21ィエD2-adrenoceptor subtype mRNAs in human renal artery, and demonstrate the distribution of receptor subtype responsible for the contraction of renal artery. RNase protection assay showed that the mean amount of αィイD21aィエD2-mRNA was much more than that of αィイD21bィエD2- or αィイD21dィエD2-mRNAs in both the main and branch renal arteries. However, the abundance of αィイD21aィエD2-mRNA in human renal artery was much less than our previous data in the prostate. By in situ hybridization, all αィイD21ィエD2 subtype mRNAs were localized in the smooth muscle cells of the tunica media of the artery, and the distribution pattern of these three mRNAs in the main artery was the same as in the branch artery. However, the intensity of signals for αィイD21dィエD2 and αィイD21bィエD2 antisense RNAs probes were lower than that for αィイD21aィエD2 antisense RNA probe. In the functional study, concentration-response curves to noradrenaline pretreated with KMD-3213, an αィイD21A/LィエD2-adrenoceptor selective antagonist, seemed to be biphasic curves. Chloroethyclonidine (CEC) failed to inactivate the noradrenaline-induced contraction and prazosin showed relatively low affinity with a pAィイD22ィエD2 value of 8.8. These data suggest that the αィイD21A/LィエD2-adrenoceptor primarily mediates those responses to noradrenaline in this artery. The other αィイD21ィエD2-adrenoceptor subtypes could also mediate the secondary contractile response to noradrenaline in this artery.
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