| Project/Area Number |
14370314
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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 |
Kidney internal medicine
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| Research Institution | Tohoku University |
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Principal Investigator |
TAKEUCHI Kazuhisa Tohoku University, Graduate School of Medicine, Associate Professor, 大学院・医学系研究科, 助教授 (40260426)
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| Co-Investigator(Kenkyū-buntansha) |
SUGAWARA Akira Tohoku University, Hospital, Lecture, 病院・講師 (90270834)
ARIMA Syuji Tohoku University, Hospital, Lecture, 病院・講師 (60323010)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥12,700,000 (Direct Cost: ¥12,700,000)
Fiscal Year 2003: ¥6,100,000 (Direct Cost: ¥6,100,000)
Fiscal Year 2002: ¥6,600,000 (Direct Cost: ¥6,600,000)
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| Keywords | Prostaglandin / Thromboxane / NaCl metabolism / Hypertension / Giltelam syndrome / angiotensin receptor / PPAR-γ / NaCl代謝 / PPAR-γ |
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| Research Abstract |
In this study period, we have investigated the role of vascular peroxisome proliferator activated-receptor ganma (PPAR-γ) in hypertensive arteriosclerosis in terms of molecular biology, physiology, and clinical science. We previously reported that PPAR-γ activation suppressed thromboxaen (TX) synthase gene. In this study, we have newly observed that PPAR-γ can also suppress TX receptor gene, as well as angiotensin type 1 receptor gene at the transcription level. In the gene transcription mechanism, transcription co-factors (CBP etc) are involved. Additionally, retinoic acid, a ligand of RXR, has also shown to suppress TX receptor gene transctription. In the physiology study, we have demonstrated that PPAR-γ ligand troglitazone dilated biphasically renal glomerular afferent and efferent arterioles, and the later phase dilatation is possibly mediated via a genomic action. PPAR-γ ligand pioglitazone has shown to increase plasma BNP levels in DM-2 patients with mild congestive heart failure. Non-genomic action of aldosterone has shown and thus a novel aldosterone action affecting NaCl metabolim via renal microcirculation has been suggested.
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