Journal
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
Volume 17, Issue 7, Pages 1791-1795Publisher
AMER SOC NEPHROLOGY
DOI: 10.1681/ASN.2006030264
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Funding
- NHLBI NIH HHS [HL-68607] Funding Source: Medline
- NIDDK NIH HHS [DK-52121] Funding Source: Medline
- PHS HHS [KD-64233] Funding Source: Medline
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An elevated serum uric acid is associated with the development of hypertension and renal disease. Renal regulation of urate excretion is largely controlled by URAT1 (SLC22A12), a member of the organic anion transporter superfamily. This study reports the specific expression of URAT1 on human aortic vascular smooth muscle cells, as assessed by reverse transcription-PCR and Western blot analysis. Expression of URAT1 was localized to the cell membrane. Evidence that the URAT1 transporter was functional was provided by the finding that uptake of C-14-urate was significantly inhibited in the presence of probenecid, an organic anion transporter inhibitor. It is proposed that URAT1 may provide a mechanism by which uric acid enters the human vascular smooth muscle cell, a finding that may be relevant to the role of uric acid in cardiovascular disease.
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