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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Imidapril improves L-NAME-exacerbated nephrosclerosis with TGF-beta 1 inhibition in spontaneously hypertensive rats.

OBJECTIVE: This study was designed to investigate whether chronic angiotensin-converting enzyme (ACE) inhibition prevents hypertensive glomerular injury and inhibits increases in the mRNA levels and immunohistological expression of the apoptosis inducer caspase-3, and transforming growth factor (TGF)-beta 1 during prolonged nitric oxide synthase (NOS) inhibition with N-nitro-L-arginine methyl ester (L-NAME) in spontaneously hypertensive rats (SHR). METHODS AND RESULTS: For 3 weeks, we studied three groups of 20-week-old male SHR: a control group, a l-NAME group, and a group treated with L-NAME and the ACE inhibitor imidapril. L-NAME rats developed severe hypertensive nephrosclerosis with significantly elevated blood pressure, markedly increased urinary protein excretion and serum creatinine levels, and more severe glomerulosclerosis and tubulo-interstitial changes. Levels of TGF-beta 1 mRNA in the renal tissue was also significantly increased in L-NAME rats compared with control SHR. Addition of imidapril significantly lowered blood pressure, inhibited nephrosclerosis and attenuated the mRNA level of TGF-beta 1 in comparison with L-NAME/SHR. Histologically, the glomerular cell apoptosis labeling index, terminal doxynucleotidil transferase-mediated dUTP nick-end labeling of fragmented DNA (TUNEL) and active caspase-3, and TGF-beta 1 positive areas were also reduced by imidapril. CONCLUSION: These data suggest that imidapril prevents glomerular and arteriolar damages and renal functions, through inhibiting both TGF-beta 1 production and apoptosis induction.[1]


  1. Imidapril improves L-NAME-exacerbated nephrosclerosis with TGF-beta 1 inhibition in spontaneously hypertensive rats. Ono, H., Saitoh, M., Ono, Y., Ishimitu, T., Matsuoka, H. J. Hypertens. (2004) [Pubmed]
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