The relationship between Vitamin D, Urate metabolism and Angiotensin II in renal proximal tubule
Date Issued
2008
Date
2008
Author(s)
Yang, Feng-Jung
Abstract
Background: olume status is linked with the function of our kidney. The body volume decreased with increasing serum uric acid level and serum calcium level due to decreasing the clearance of both. Angiotensin II increased proximal tubule sodium reabsorption. Losartan, a kind of angiotensin type I receptor, AT1R blocker has hypouricemia effect. vitamin D receptor has the effect on the renal distal tubule of calcium metabolism. Reports relating hyperuricemia and hypertension have been filed for many decades. Nevertheless, controversy remains concerning serum uric acid concentration as an independent risk factor underlying coronary heart disease (CHD) and essential hypertension or as an indirect marker of renovascular involvement.Recent studies showed VDR and uric acid are prognostic factors in chronic kidney disease. Renal renin-angiotensin system may play a role in hyperuricemia and cardiovascular negative factor. his study is designed to clarify the interaction among Ang II, Vitamin D receptor, uric acid transporter. The immortalized human kidney (HK-2) cell line used during this work is of proximal tubule origin and was originally isolated from a normal human kidney.ethods: uman proximal tubular cells were cultured in hormonally defined medium. Cells at 80% confluency were exposed to Angiotensin II for 1-24 hours. Activity and expression of URAT-1 was examined by PCR and Western blot analysis. Activity and expression of VDR was examined by PCR and Western blot analysis also.esults:ngiotensin II resulted in a dose-dependent increase in the expression of VDR/URAT-1. AT1 antagonist provided the suppression but showed without significant suppression of Ang II effect. AT2 antagonist provided the augmentation but showed without significant ehancement of Ang II effectonclusion: he effects of rennin-angiotension system on proximal tubular URAT-1/VDR expression are mediated through the pathway of Angiotensin II. Angiotensin II can up-regulate the URAT-1/VDR and be suppressed with Angiotension II receptor type I blocker. To These findings may provide new insights into the role of RAS system in the development and possible therapeutic intervention in hyperuricemia and CKD.
Subjects
URAT-1
uric acid
Vit D
Vit D receptor
CKD
Angiotensin II
renal proximal tubule cel
SDGs
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