2004 Fiscal Year Final Research Report Summary
Molecular Biological Studies on Relationships between Changes in Renal Tubular Transporter Gene Expressions and Deterioration of Drug Excretory Functions in Renal Diseases
| Project/Area Number |
14370781
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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 |
応用薬理学・医療系薬学
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| Research Institution | Kumamoto University |
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Principal Investigator |
SAITO Hideyuki Kumamoto University, Hospital Pharmacy, Professor, 医学部附属病院, 教授 (40225727)
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| Co-Investigator(Kenkyū-buntansha) |
HAMADA Akinobu Kumamoto University, Hospital Pharmacy, Lecturer, 医学部附属病院, 講師 (00322313)
MASUDA Satohiro Kyoto University, Graduate School of Medicine, Lecturer, 医学研究科, 講師 (90303825)
FUKATSU Atsushi Kyoto University, Graduate School of Medicine, Lecturer, 医学研究科, 講師 (90247685)
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| Project Period (FY) |
2002 – 2004
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| Keywords | Drug transporter / Renal excretion / Renal tubular dysfunction / Nephrotoxicity / Dosage regimen / Renal failure |
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| Research Abstract |
The proximal tubules of kidney play a pivotal role in limiting or preventing toxicity by secreting organic anions and cations into urine. Organic ion transporter family(SLC22A) appeared to mediate renal secretion of these molecules. Organic anion transporters, OAT-K1 and OAT-K2 could serve as multispecific transporters, mediating transport of a wide variety of endogenous substances and xenobiotics. The levels of urinary excretion of dmetidine was reduced under cronic renal failure(CRF) partiy due to the reduced expression of rOCT2, and the lowered plasma level of testosterone was suggested to be responsible for the depressed rOCT2 expression in CRF. hOAT3 was suggested to play an important role for anionic drug secretion in patients with renal diseases and that the expression levels of drug transporters may be related to the alteration of renal drug secretion.
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Research Products
(19 results)
