Silent partner in blood vessel homeostasis? Pervasive role of nitric oxide in vascular disease Academic Article uri icon

Overview

MeSH Major

  • Aorta
  • Cyclooxygenase 2
  • Inflammation
  • Mitogen-Activated Protein Kinases
  • Muscle, Smooth, Vascular
  • Myocytes, Smooth Muscle
  • Nitric Oxide Synthase Type II

abstract

  • The endothelium generates powerful mediators that regulate blood flow, temper inflammation and maintain a homeostatic environment to prevent both the initiation and progression of vascular disease. Nitric oxide (NO) is arguably the single most influential molecule in terms of dictating blood vessel homeostasis. In addition to direct effects associated with altered NO production (e.g. vasoconstriction, excessive inflammation, endothelial dysfunction), NO is a critical modulator of vaso-relevant pathways including cyclooxygenase (COX)-derived prostaglandin production and angiotensin II generation by the renin-angiotensin system. Furthermore, NO may influence the selectivity of COX-2 inhibitors and ultimately contribute to controversies associated with the use of these drugs. Consistent with a central role for NO in vascular disease, disruptions in the production and bioavailability of NO have been linked to hypertension, diabetes, hypercholesterolemia, obesity, aging, and smoking. The ability of the vessel wall to control disease-associated oxidative stress may be the most critical determinant in maintaining homeostatic levels of NO and subsequently the prospect of stroke, myocardial infarction and other CV abnormalities. To this end, investigation of mechanisms that alter the balance of protective mediators, including pathways that are indirectly modified by NO, is critical to the development of effective therapy in the treatment of CV disease.

publication date

  • November 2009

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC2847292

Digital Object Identifier (DOI)

  • 10.2174/157340209789587726

PubMed ID

  • 20368751

Additional Document Info

start page

  • 273

end page

  • 282

volume

  • 5

number

  • 4