Impaired angiogenesis in the enalapril-treated neonatal rat kidney.
- Author:
Hyung Eun YIM
1
;
Kee Hwan YOO
;
Eun Soo BAE
;
Young Sook HONG
;
Joo Won LEE
Author Information
- Publication Type:Original Article
- Keywords: Angiotensin II; Growth and development; Vascular remodeling
- MeSH: Angiotensin II; Animals; Blotting, Western; Capillaries; Enalapril; Endothelial Cells; Eosine Yellowish-(YS); Growth and Development; Hematoxylin; Humans; Infant, Newborn; Kidney*; Parturition; Platelet-Derived Growth Factor; Rats*; Receptors, Vascular Endothelial Growth Factor; Vascular Endothelial Growth Factor A
- From:Korean Journal of Pediatrics 2016;59(1):8-15
- CountryRepublic of Korea
- Language:English
- 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-beta 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-beta 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.
