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Impaired angiogenesis in the enalapril-treated neonatal rat kidney

Authors
Yim, H.E.Yoo, K.H.Bae, E.S.Hong, Y.S.Lee, J.W.
Issue Date
2016
Publisher
Korean Pediatric Society
Keywords
Angiotensin II; Growth and development; Vascular remodeling
Citation
Korean Journal of Pediatrics, v.59, no.1, pp.8 - 15
Indexed
SCOPUS
KCI
Journal Title
Korean Journal of Pediatrics
Volume
59
Number
1
Start Page
8
End Page
15
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/91397
DOI
10.3345/kjp.2016.59.1.8
ISSN
1738-1061
Abstract
Purpose: Nephrogenesis is normally accompanied by a tightly regulated and efficient vascularization. We investigated the effect of angiotensin II inhibition on angiogenesis in the developing rat kidney. Methods: Newborn rat pups were treated with enalapril (30 mg/kg/day) or vehicle (control) for 7 days after birth. Renal histological changes were checked using Hematoxylin & Eosin staining. We also investigated the intrarenal expression of vascular endothelial growth factor (VEGF)-A, VEGF receptor 1 (VEGFR1), VEGFR2, platelet-derived growth factor (PDGF)-B, and PDGF receptor-β with Western blotting and immunohistochemical staining at postnatal day 8. Expression of the endothelial cell marker CD31 was examined to determine glomerular and peritubular capillary density. Results: Enalapril-treated rat kidneys showed disrupted tubules and vessels when compared with the control rat kidneys. In the enalapril-treated group, intrarenal VEGF-A protein expression was significantly higher, whereas VEGFR1 protein expression was lower than that in the control group (P<0.05). The expression of VEGFR2, PDGF-B, and PDGF receptor-β was not different between the 2 groups. The increased capillary CD31 expression on the western blots of enalapril-treated rat kidneys indicated that the total endothelial cell protein level was increased, while the cortical capillary density, assessed using CD31 immunohistochemical staining, was decreased. Conclusion: Impaired VEGF-VEGFR signaling and altered capillary repair may play a role in the deterioration of the kidney vasculature after blocking of angiotensin II during renal development. © 2016 by The Korean Pediatric Society.
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