Role of Mitochondria-derived Oxidative Stress on Microvascular Endothelial Function in Healthy Non-Hispanic Black and White Adults

Summary

Cardiovascular disease (CVD) is a leading cause of morbidity and mortality worldwide, and the non-Hispanic Black (NHB) population is disproportionately affected. Our research has previously demonstrated that oxidative stress may contribute to reduced vascular function in otherwise healthy NHB adults, potentially predisposing them to the development of hypertension and CVD. This study is designed to examine whether the mitochondria are an important source of oxidative stress-induced vascular dysfunction in healthy NHB adults.

Eligibility

Age range

18–75 years

Sex

All

Healthy volunteers

Yes

Interventions

• Dietary Supplement
  MitoQ

  MitoQ supplement is composed of mitoquinol mesylate, which is a synthetic analog of coenzyme Q10

• Dietary Supplement
  Placebo

  MitoQ matched Placebo

• Drug
  MitoTempo

  During each experimental visit, intradermal microdialysis will be used to locally infuse MitoTempo (a mitochondria-specific superoxide dismutase mimetic) into the cutaneous microvasculature in the ventral aspect of the left forearm.

• Drug
  Tempol

  During each experimental visit, intradermal microdialysis will be used to locally infuse Tempol (a superoxide dismutase mimetic) into the cutaneous microvasculature in the ventral aspect of the left forearm.

• Drug
  L-NAME

  During each experimental visit, L-NAME (nitric oxide synthase inhibitor) will be perfused through microdialysis fibers for quantification of nitric oxide-mediated vasodilation.

• Drug
  SNP - Sodium Nitroprusside

Location