Physiological and Pathophysiological Relevance of Nitric Oxide Synthases (NOS) in Retinal Blood Vessels

Front Biosci (Landmark Ed). 2024 May 16;29(5):190. doi: 10.31083/j.fbl2905190.

Abstract

Nitric oxide synthases (NOS) are essential regulators of vascular function, and their role in ocular blood vessels is of paramount importance for maintaining ocular homeostasis. Three isoforms of NOS-endothelial (eNOS), neuronal (nNOS), and inducible (iNOS)-contribute to nitric oxide production in ocular tissues, exerting multifaceted effects on vascular tone, blood flow, and overall ocular homeostasis. Endothelial NOS, primarily located in endothelial cells, is pivotal for mediating vasodilation and regulating blood flow. Neuronal NOS, abundantly found in nerve terminals, contributes to neurotransmitter release and vascular tone modulation in the ocular microvasculature. Inducible NOS, expressed under inflammatory conditions, plays a role in response to pathological stimuli. Understanding the distinctive contributions of these NOS isoforms in retinal blood vessels is vital to unravel the mechanisms underlying various ocular diseases, such diabetic retinopathy. This article delves into the unique contributions of NOS isoforms within the complex vascular network of the retina, elucidating their significance as potential therapeutic targets for addressing pathological conditions.

Keywords: blood vessels; endothelium; nitric oxide synthase; retina.

Publication types

  • Review

MeSH terms

  • Animals
  • Diabetic Retinopathy / enzymology
  • Diabetic Retinopathy / metabolism
  • Diabetic Retinopathy / physiopathology
  • Humans
  • Nitric Oxide / metabolism
  • Nitric Oxide Synthase Type I / metabolism
  • Nitric Oxide Synthase Type II / metabolism
  • Nitric Oxide Synthase Type III / metabolism
  • Nitric Oxide Synthase* / metabolism
  • Retinal Vessels* / metabolism
  • Retinal Vessels* / physiopathology

Substances

  • Nitric Oxide Synthase
  • Nitric Oxide Synthase Type III
  • Nitric Oxide Synthase Type I
  • Nitric Oxide
  • Nitric Oxide Synthase Type II