Background: The senescence programme is implicated in diverse pathophysiological processes, including embryonic development and tissue regeneration. Senescent cells that are acutely present are beneficial during renal development and repair, whereas aberrant accumulation of senescent cells promotes kidney disease. In this study, we aimed to investigate the effect of renin angiotensin system (RAS) block on renal cell senescence in the developing rat kidney. Methods: Newborn rat pups were treated with enalapril (30 mg/kg) or vehicle for 7 days after birth. We investigated the intrarenal expression of cell cycle regulators p21 and p16 with Western blotting and immunohistochemistry at postnatal day 8. For the determination of renal cellular senescence, immunostaining for senescence-associated β-galactosidase (SA-β-gal) and telomerase reverse transcriptase (TERT) was also assessed. Results: Enalapril-treated rats showed significant alterations in renal architecture, including tubular injury. In the enalapril-treated group, intrarenal p16 and p21 protein expression was decreased, compared to the controls ( P 0.05). Immunohistochemistry for p21 and p16 showed reduced cortical immunostaining in the enalapril-treated kidneys. The immunoreactivity of TERT in enalapril-treated kidneys was weaker than that in control kidneys ( P 0.05). Control kidneys revealed a clear positive SA-β-gal signal in the cortical tubules and SA-β-gal activity was noticeably lower in the enalapril-treated kidneys than in control kidneys ( P 0.05). Conclusion: The RAS may involve developmentally programmed renal cell senescence during kidney development, and impaired renal cell senescence together with decreased activity of p21, p16, and TERT can contribute to kidney injury by the RAS inhibition in developing rat kidney.