Exaggerated Alpha‐1 Adrenoreceptor Mediated Vasoconstriction in Young Black Men is not Influenced by Superoxide‐Mediated Oxidative Stress

Abstract

Black individuals (BL) have a greater risk for hypertension and cardiovascular disease than other populations, the cause of which is likely multifactorial. However, vascular dysfunction appears to be a key preceding factor to the racial disparities observed. This observation has been demonstrated in young, otherwise healthy BL. Our group recently demonstrated that young BL men (BM) exhibit exaggerated sympathetic vascular transduction (SVT), i.e., greater vasoconstriction and pressor responses to spontaneous bursts of sympathetic nerve activity, at rest compared to young white men (WM). This response may be mediated by elevated oxidative stress, which may be 1) reducing nitric oxide (NO) bioavailability and subsequent vasodilatory capacity and/or 2) directly affecting blood vessel reactivity. In this regard, previous literature has established that young BM have elevated oxidative stress and reduced NO bioavailability relative to other populations. Whether these conditions contribute to increased SVT in BM is currently unknown. Accordingly, this study tested the hypothesis that BM have an exaggerated vasoconstrictor response to the selective α1‐adrenoreceptor agonist phenylephrine (PE) compared to WM which is augmented by elevated oxidative stress. To test this hypothesis, four intradermal microdialysis membranes were placed in the dorsal forearm of 3 WM and 6 BM (mean ± SD; age: 24±5 vs. 22±3 y) and the skin blood flow (SkBF) responses to intradermal infusion of PE were assessed. Following trauma resolution, each site received one of four infusions for 30‐min: lactated Ringer's (control), apocynin (NADPH oxidase inhibitor; 100 μM), allopurinol (xanthine oxidase inhibitor; 10 μM), or tempol (superoxide scavenger; 10 μM). Each site was then locally heated to 33°C for 10‐min to establish baseline SkBF. Each site then received a coinfusion of PE (100 mM) for 6‐min to elicit vasoconstriction, with the response presented as a percent reduction in cutaneous vascular conductance (CVC; flux/mean arterial pressure) from baseline (%CVCB). Following PE administration, BM exhibited exaggerated vasoconstriction compared to WM (control: −69.0±16.5 vs. −34.8±15.2 %CVCB; apocynin: −58.1±18.3 vs. −43.5± 2.4 %CVCB; allopurinol: −59.2±13.1 vs. −53.5±23.3 %CVCB; tempol: −63.5±18.1 vs. −37.7±16.7 %CVCB; main effect: P < 0.01). However, no interaction effect was observed for the race‐by‐site comparison (P = 0.35), suggesting no effect of the drugs used across races. In conclusion, these preliminary data suggest that BM exhibit exaggerated α1‐adrenoreceptor‐mediated vasoconstriction compared to WM, which is consistent with previous literature. Furthermore, these preliminary findings indicate this response is not superoxide‐mediated, suggestive of a different, currently unknown controlling mechanism for exaggerated vasoconstriction.Support or Funding InformationUTA Start‐up funds to R. Matthew BrothersThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.