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Retinal neovascularization is prevented by blockade of the renin-angiotensin system

C J Moravski1, D J Kelly, M E Cooper

  • 1Department of Physiology, The University of Melbourne, Parkville, Victoria, Australia.

Hypertension (Dallas, Tex. : 1979)
|January 11, 2000
PubMed

Insights

Blocking the renin-angiotensin system with ACE inhibitors like lisinopril may prevent blood vessel growth in retinopathy. This suggests potential retinoprotective benefits for proliferative retinopathy.

Area of Science:

  • Ophthalmology
  • Cardiovascular Research
  • Molecular Biology

Background:

  • Angiotensin II and vascular endothelial growth factor (VEGF) are implicated in proliferative diabetic retinopathy.
  • Retinal neovascularization is a key feature of proliferative retinopathies.

Purpose of the Study:

  • To investigate the role of the renin-angiotensin system (RAS) in retinal neovascularization.
  • To evaluate the effects of RAS blockers on retinopathy of prematurity in a rat model.

Main Methods:

  • Used neonatal transgenic (mRen-2)27 rats and Sprague-Dawley rats to model retinopathy of prematurity.
  • Administered ACE inhibitor (lisinopril) and angiotensin type 1 receptor antagonist (losartan).
  • Assessed retinal renin levels, blood vessel growth, and expression of VEGF and its receptor using in situ hybridization.

Main Results:

  • Both lisinopril and losartan increased retinal renin and prevented inner retinal blood vessel growth.
  • Retinopathy of prematurity increased VEGF and VEGF receptor type 2 mRNA expression.
  • Lisinopril reduced VEGF and VEGF receptor type 2 mRNA, while losartan had no effect.

Conclusions:

  • Inhibition of the renin-angiotensin system, particularly with ACE inhibitors, shows promise in preventing retinal neovascularization.
  • VEGF signaling is involved in the pathogenesis of retinopathy of prematurity.
  • RAS-targeting agents may serve as retinoprotective therapies for proliferative retinopathies.

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