Angiotensin-converting enzyme inhibition aggravates renal interstitial injury resulting from partial unilateral ureteral obstruction in the neonatal rat.

@article{Chen2007AngiotensinconvertingEI,
  title={Angiotensin-converting enzyme inhibition aggravates renal interstitial injury resulting from partial unilateral ureteral obstruction in the neonatal rat.},
  author={Christina O Chen and Matthew H Park and Michael S. Forbes and Barbara A. Thornhill and Susan C. Kiley and Kee Hwan Yoo and Robert L. Chevalier},
  journal={American journal of physiology. Renal physiology},
  year={2007},
  volume={292 3},
  pages={
          F946-55
        }
}
Congenital urinary tract obstruction is the most important cause of renal insufficiency in infants and children, and angiotensin-converting enzyme (ACE) inhibitors attenuate the progression of renal disease in adults. ACE inhibitors are increasingly utilized in children with progressive renal disease. Because angiotensin is necessary for normal renal development, we examined the effects of ACE inhibition both during and immediately following the period of postnatal nephrogenesis in the neonatal… 
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Angiotensin AT1-receptor inhibition exacerbates renal injury resulting from partial unilateral ureteral obstruction in the neonatal rat.
TLDR
It is concluded that selective inhibition of AT(1) receptors during nephrogenesis (but not during subsequent renal maturation) exacerbates injury to the obstructed kidney and also injures the contralateral kidney.
Effect of unilateral ureteral obstruction and anti-angiotensin II treatment on renal tubule and interstitial cell apoptosis in rats.
AT1 receptor blockade prevents interstitial and glomerular apoptosis but not fibrosis in pigs with neonatal induced partial unilateral ureteral obstruction.
TLDR
It is demonstrated that ANG II plays a role in PUUO-induced glomerular cell apoptosis, suggesting that pathways not involving AT(1) receptor stimulation contribute to neonatal obstruction-induced fibrosis or that prevention of interstitialcell apoptosis counteracts a potential antifibrotic effect of AT( 1) receptor blockade in this pig model of congenital obstructive nephropathy.
Effect of unilateral ureteral obstruction and anti-angiotensin II treatment on renal tubule and interstitial cell apoptosis in rats.
TLDR
It is hypothesized that both ACE inhibitor (cilazapril) and AT1 receptor antagonist (losartan) would decrease renal tubular and interstitial apoptosis, and that cilazaprill would have greater antiapoptotic effect than losartan.
Transforming growth factor-β1 receptor inhibition preserves glomerulotubular integrity during ureteral obstruction in adults but worsens injury in neonatal mice.
TLDR
The results indicate that while caution is necessary in treating congenital uropathies, ALK5 inhibitors may prevent nephron loss due to adult kidney disease and TGF-β1 inhibition aggravates obstructive injury in neonates.
Effect of Angiotensin II and Small GTPase Ras Signaling Pathway Inhibition on Early Renal Changes in a Murine Model of Obstructive Nephropathy
TLDR
Assessment of the effect of inhibiting angiotensin II receptors or Ras activation on early renal fibrotic changes induced by UUO shows that pharmacological inhibition of Ras activation may hold promise as a future strategy in the prevention of renal fibrosis.
Protein kinase C inhibitor chelerythrine attenuates partial unilateral ureteral obstruction induced kidney injury in neonatal rats
Ureteral obstruction as a model of renal interstitial fibrosis and obstructive nephropathy.
TLDR
The UUO model is likely to reveal useful biomarkers of progression of renal disease, as well as new therapies, which are desperately needed to allow intervention before the establishment of irreversible renal injury.
The therapeutic approaches of renal recovery after relief of the unilateral ureteral obstruction: A comprehensive review
TLDR
The therapeutic procedure of renal recovery after the RUUO situation in human and animal studies is focused on, with particular attention to the post-RUUO periods.
Mechanisms of renal injury and progression of renal disease in congenital obstructive nephropathy
TLDR
The cellular and molecular events responsible for obstructive injury to the developing kidney have been elucidated from animal models and revealed nephron loss through cellular phenotypic transition and cell death, leading to the formation of atubular glomeruli and tubular atrophy.
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References

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