Local Antioxidant Therapy Vasoconstriction Effects in Different Races
Status:
Recruiting
Trial end date:
2021-08-31
Target enrollment:
Participant gender:
Summary
Cardiovascular disease (CVD) afflicts nearly one-third of the adult population with all races
and ethnicities represented in CVD prevalence. Unfortunately, a disparity exists such that
the black population (BL) is disproportionately affected compared to other groups, including
the white population (WH). While the underlying cause of this disparity is multifactorial,
vascular dysfunction (i.e., impaired vasodilation and/or augmented vasoconstriction) is a key
contributor. As has been previously observed, BL exhibit a heightened vasoconstrictor
response to both pharmacological (e.g., alpha-adrenergic receptor agonists) and environmental
(e.g., cold pressor test) stimuli compared to their WH counterparts. Additionally, reactive
oxygen species (ROS) and the subsequent reduction in nitric oxide (NO) bioavailability may
partially mediate this response. Our laboratory has recently observed (UTA IRB 2016-0268)
that the small blood vessels in the skin (cutaneous microvasculature) in BL, but otherwise
healthy individuals, produce an impaired blood flow response to local heating when compared
to age-, body mass index (BMI)-, and gender-matched WH. However, pre-treatment of the
cutaneous microvasculature with various antioxidants abolishes this skin blood flow
difference. These antioxidant drugs inhibit possible sources of ROS, which, as mentioned,
maybe mediating the heightened vasoconstrictor response in BL. However, this has not been
investigated in this population and thus remains unknown. Therefore, the purpose of this
study proposal is to test the following hypotheses: 1) BL will have a greater reduction in
cutaneous blood flow in response to local administration of Norepinephrine (alpha1-adrenergic
and alpha 2-adrenergic receptor agonist) relative to WH. 2) This greater reduction in the BL
population will be related to elevated oxidative stress and subsequent reduction in
bioavailability of the potent vasodilator Nitric oxide.