Pathogenesis of diabetic retinopathy and the renin-angiotensin system

Ophthalmic Physiol Opt. 2003 Nov;23(6):495-501. doi: 10.1046/j.1475-1313.2003.00134.x.

Abstract

Despite the beneficial effects of good glycaemic control, loss of vision because of diabetic retinopathy (DR) still occurs. Recent studies have suggested that hypertension is a risk factor for the development and progression of DR and that blood pressure reduction can delay the progression of retinopathy. The renin-angiotensin system is activated by chronic hyperglycaemia, and the vitreous fluid level of angiotensin II (AII) is elevated in patients with proliferative diabetic retinopathy and diabetic macular oedema. AII increases vascular permeability and promotes neovascularization. It has been suggested that an autocrine-paracrine relationship may exist between AII and vascular endothelial growth factor in the ocular tissues. Accordingly, angiotensin-converting enzyme inhibitors or AII Type 1 (AT1) receptor blockers may be useful therapeutic agents for preventing the progression of DR.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Angiotensin II / metabolism
  • Angiotensin-Converting Enzyme Inhibitors / metabolism
  • Diabetic Retinopathy / etiology*
  • Diabetic Retinopathy / physiopathology
  • Disease Progression
  • Humans
  • Hyperglycemia / complications
  • Hyperglycemia / physiopathology
  • Hypertension / complications
  • Hypertension / physiopathology
  • Macular Degeneration / etiology
  • Macular Degeneration / physiopathology
  • Receptors, Angiotensin / metabolism
  • Renin-Angiotensin System / physiology*
  • Risk Factors
  • Vascular Endothelial Growth Factors

Substances

  • Angiotensin-Converting Enzyme Inhibitors
  • Receptors, Angiotensin
  • Vascular Endothelial Growth Factors
  • Angiotensin II