ArticlePediatric nephrology (Berlin, Germany)2006
AT1 antagonist modulates activin-like kinase 5 and TGF-beta receptor II in the developing kidney.
Article in Pediatric nephrology (Berlin, Germany), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 11 citations in OpenAlex.
- Impaired angiogenesis in the enalapril-treated neonatal rat kidney.Korean journal of pediatrics · 2016Article
- Angiotensin II receptor type 1 blockade decreases CTGF/CCN2-mediated damage and fibrosis in normal and dystrophic skeletal muscles.Journal of cellular and molecular medicine · 2012Article
- Endothelin A receptor blockade influences apoptosis and cellular proliferation in the developing rat kidney.Journal of Korean medical science · 2009Article
- Severe anemia caused by the angiotensin receptor blocker irbesartan after renal transplantation.Pediatric nephrology (Berlin, Germany) · 2007Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
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Abstract
Previous studies by our group have demonstrated that angiotensin-converting enzyme (ACE) inhibition in the developing kidney modulates transforming growth factor-beta receptors. Blocking of angiotensin II (ANG II) mainly through angiotensin II type 1 receptor (AT1) has been implicated in mediating this ACE inhibition. The present study was designed to investigate the effects of an AT1 antagonist, losartan, on transforming growth factor-beta1 (TGF-beta1), TGF-beta receptor I [TbetaRI, activin-like kinase (ALK)-1, ALK-5], TGF-beta receptor II (TbetaRII), and alpha-smooth muscle actin (alpha-SMA) expression in the developing kidney. Newborn rat pups were treated with losartan (30 mg/kg per day) or normal saline for 7 days. Kidneys were removed for immunohistochemistry, reverse transcription polymerase chain reaction (PCR), and Western blotting of TGF-beta1, ALK-1, ALK-5, TbetaRII, and alpha-SMA. Renal ALK-5 and TbetaRII protein expressions in the losartan-treated group were found to be significantly increased (P<0.05), whereas TGF-beta1, ALK-1, and alpha-SMA protein expressions were not changed by losartan treatment. The losartan-treated group also showed significantly increased mean tubular diameter and interstitial area of the kidney (P<0.05). These results suggest that AT1 inhibition in the developing kidney impairs renal growth and development and modulates the expression of ALK-5 and TbetaRII.
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