Abstract:
BACKGROUND:Chronic metabolic acidosis is a common metabolic disturbance and its clinical impact can be severe and extensive. The role and the change of the intrarenal renin-angiotensin system (RAS) during metabolic acidosis are uncertain, and whether acidosis can evoke inflammation remains unclear. METHODS:Male Sprague-Dawley rats were fed with water containing 0.14 M NH(4)Cl to induce metabolic acidosis for 1 and 8 weeks, respectively. They were compared with animals fed with deionized water (control) and equimolar sodium chloride water (NaCl). Gene expression analysis of RAS components included renin, renin/prorenin receptor, angiotensinogen, angiotensin-converting enzyme (ACE), and angiotensin II type 1 and 2 receptors (AT1R and AT2R). Histological examination was also performed to detect morphological change. RESULTS:Acidosis was found in 1-week NH(4)Cl-treated rats but not in the 8-week group. More than twofold proteinuria and a significant decline of glomerular filtration rate (GFR) were observed in acid-loaded rats. Compared to the control and NaCl groups, angiotensinogen, ACE, AT1R and AT2R were significantly increased in the 1-week acidosis group (all p < 0.05). Sustained increase of AT1R expression was found as NH(4)Cl was continued for 8 weeks. There was no significant change in transforming growth factor-β and nuclear factor-κB. The architecture of tubular epithelial cells was affected during our experiment. CONCLUSION:Metabolic acidosis induced proteinuria and decline of GFR in association with activation of intrarenal RAS.
journal_name
Am J Nephroljournal_title
American journal of nephrologyauthors
Ng HY,Chen HC,Tsai YC,Yang YK,Lee CTdoi
10.1159/000328742subject
Has Abstractpub_date
2011-01-01 00:00:00pages
55-63issue
1eissn
0250-8095issn
1421-9670pii
000328742journal_volume
34pub_type
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journal_title:American journal of nephrology
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