Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Free radicals in diabetic endothelial cell dysfunction

B Tesfamariam1

  • 1Department of Pharmacology, Bristol-Myers Squibb Research Institute, Princeton, NJ 08543.

Free Radical Biology & Medicine
|March 1, 1994
PubMed
Summary

Diabetic arteries show impaired relaxation due to prostaglandin H2 and superoxide anion generation. Treatments targeting these pathways, like prostaglandin receptor blockade, can restore normal function.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Arylpropanolamines: selective beta3 agonists arising from strategies to mitigate phase I metabolic transformations.

Bioorganic & medicinal chemistry letters·2007
Same author

BMS-201620: a selective beta 3 agonist.

Bioorganic & medicinal chemistry letters·2004
Same author

Beta 3 agonists. Part 1: evolution from inception to BMS-194449.

Bioorganic & medicinal chemistry letters·2001
Same author

BMS-196085: a potent and selective full agonist of the human beta(3) adrenergic receptor.

Bioorganic & medicinal chemistry letters·2001
Same author

Quantitation of tremor in response to beta-adrenergic receptor stimulation in primates: relationship with hypokalemia.

Journal of pharmacological and toxicological methods·1999
Same author

Differential effects of pravastatin, simvastatin, and atorvastatin on Ca2+ release and vascular reactivity.

Journal of cardiovascular pharmacology·1999

Area of Science:

  • Vascular Biology
  • Endocrinology
  • Oxidative Stress

Background:

  • Diabetes mellitus is associated with impaired endothelium-dependent relaxations and increased vasoconstrictor prostanoids in arteries.
  • These vascular abnormalities are observed in both diabetic animals and humans.

Purpose of the Study:

  • To review the cumulative effects of oxidative stress on diabetic endothelial cell dysfunction.
  • To explore the interrelationship between cyclooxygenase catalysis, protein kinase C activity, and polyol pathway flux in diabetes.

Main Methods:

  • Analysis of studies investigating prostaglandin (PG) H2/thromboxane A2 receptor blockade and superoxide dismutase effects.
  • Examination of mechanisms involving prostaglandin H2, superoxide anion (O2-.), and NADPH depletion in endothelial cells.
  • Review of how elevated glucose, oxygen-derived free radicals, and protein kinase C activation impact endothelial function.

Main Results:

  • Prostaglandin H2 and/or superoxide anion generation contribute to vascular abnormalities in diabetes.
  • Elevated glucose exacerbates these effects via increased aldose reductase activity, leading to NADPH depletion and reduced nitric oxide formation.
  • Common mechanisms, including oxidative stress, protein kinase C activation, and polyol pathway flux, impair endothelial cell function in diabetes.

Conclusions:

  • Oxidative stress plays a critical role in diabetic endothelial dysfunction.
  • Interventions targeting prostaglandin pathways and oxidative stress show potential for restoring vascular function in diabetes.
  • Understanding the interplay between cyclooxygenase, protein kinase C, and the polyol pathway is crucial for managing diabetic vascular complications.

Related Experiment Videos