May 2005
Volume 46, Issue 13
ARVO Annual Meeting Abstract  |   May 2005
Captopril Inhibits Acellular Capillary Formation in Diabetic Retinopathy
Author Affiliations & Notes
  • J. Zhang
    Ophthalmology, Case Western Reserve Univ, Cleveland, OH
  • X. Xi
    Ophthalmology, Case Western Reserve Univ, Cleveland, OH
  • L. Gao
    Ophthalmology, Case Western Reserve Univ, Cleveland, OH
  • Footnotes
    Commercial Relationships  J. Zhang, None; X. Xi, None; L. Gao, None.
  • Footnotes
    Support  NIH grant EY14154, ADA
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 431. doi:
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      J. Zhang, X. Xi, L. Gao; Captopril Inhibits Acellular Capillary Formation in Diabetic Retinopathy . Invest. Ophthalmol. Vis. Sci. 2005;46(13):431.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Purpose: The angiotensin–converting enzyme inhibitors (ACE inhibitor) are one of the few drugs that have been identified by clinical studies to inhibit diabetic retinopathy, but the mechanism underlying the action is unclear, especially since the beneficial effect is observed even in the absence of hypertension. This study was conducted to examine the effect of ACE inhibitors on microvascular pathogenesis in retinas in diabetes. Methods: Rats were made experimentally diabetic by injection of streptozotocin and treated with captopril (25 mg/kg body weight per day) for 8 months. Rat retinal endothelial cells were cultured in medium containing either 5.5 or 25 mM glucose and treated with different concentrations of captopril or losartan for 5 days. Acellular capillary formation in the retina was evaluated by trypsin–digest technique. Expression of intercellular adhesion molecule ICAM1 in retinal endothelial cells was determined by Western blot analysis. Results: Treatment of rats with captopril inhibited diabetes–induced acellular capillary formation in the retina by 85% (P < 0.05) compared with the diabetic control. Culture of retinal endothelial cells in elevated glucose upregulated ICAM1 expression by 68% (P < 0.01), and captopril significantly blocked it. This inhibitory effect was likely to be mediated by AT1 receptor since losartan also significantly inhibited elevated glucose induced upregulation of ICAM1. Conclusions: It has been demonstrated recently that chronic inflammation is responsible for many of the vascular lesions of diabetic retinopathy including capillary cell death and acellular capillary formation. Our preliminary data show that ACE inhibitors prevent retinas from diabetes–induced microvascular damages, which is at least in part mediated by their anti–inflammatory effect.

Keywords: diabetic retinopathy • inflammation 

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