| Project/Area Number |
16300136
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Laboratory animal science
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| Research Institution | Shimane University |
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Principal Investigator |
NABIKA Toru Shimane University, Faculty of Medicine, Professor, 医学部, 教授 (50180534)
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| Co-Investigator(Kenkyū-buntansha) |
IKEDA Kastumi Mukogawa Women's University, Human Environmental Sciences, Professor, 生活環境学部, 教授 (80273499)
KATOU Norihiro Research Institute, International Medical Center of Japan, Director, 部長 (80293934)
越智 弘 島根大学, 医学部, 助教授 (80204220)
権田 辰夫 総合科学研究支援センター, 実験動物分野, 助教授 (40116398)
渡邊 武 大塚GEN研究所, 所長
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥15,200,000 (Direct Cost: ¥15,200,000)
Fiscal Year 2005: ¥4,900,000 (Direct Cost: ¥4,900,000)
Fiscal Year 2004: ¥10,300,000 (Direct Cost: ¥10,300,000)
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| Keywords | essential hypertension / Spontaneously Hypertensive Rats / quantitative trait locus / 本態性高血圧 |
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| Research Abstract |
Previous reports of our laboratory showed that a quantitative trait locus (QTL) for blood pressure is located on rat chromosome 1.The evaluation of a congenic strain targeting this QTL indicated that the responsible gene(s) was in 80Mbp region. This region was still quite large and therefore it should be cut down into smaller regions to identify the responsible genes. In the process of developing the spontaneously hypertensive rats (SHR), several substrains of SHR and the stroke-prone SHR (SHRSP) have been developed and maintained for more than 20 years. As they are expected to share the same ‘hypertension' genes with each other, we hypothesized that the choromosomal fragment around the ‘hypertension' genes harbored a cluster of SSR markers that are polymorphic between SHR substrains and Wistar-Kyoto rat (WKY) substrains ; one allele of such an SSR was commonly shared in the substrains of SHR while another was observed in WKY substrains.
In this study, we therefore genotyped 270 SSR mar
… More
kers distributed densely in the chromosome-1 QTL region. Results indicated that two small fragments (3Mbp) in the region harbored clusters of SSR markers polymorphic between WKY substrains and SHR/SHRSP substrains. These regions are potential candidates having the genes responsible for the blood pressure difference between SHR (and SHRSP) and WKY. We found another fragment with 7Mbp that harbors SSR markers polymorphic between SHRSP substrains and SHR/WKY substrains. This region may account for the difference of blood pressure between SHR and SHRSP, which was indicated by a QTL analysis between SHRSP and SHR as well. We additionally evaluated blood pressure in SHR and SHRSP substrains with the telemetry system. The result indicated that all of SHR/SHRSP substrains had higher blood pressure than did WKY. However, difference of blood pressure among the substrains was significant as well ; some substrains had greater blood pressure than others. According to the genotyping result, no regions in the QTL could account for this inter-substrain difference of blood pressure. QTLs outside of the one on chromosome-1 may be responsible for this difference. Less
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