(756.2) Resting Sympathetic Transduction in Young Healthy non-Hispanic Black Women: Potential Race and Sex Differences

Poster Board Number: E447

Brandi Stephens (University of Texas at Arlington), Benjamin Young (University of Texas at Arlington), Damsara Nandadeva (University of Texas at Arlington), Rachel Skow (University of Texas at Arlington), Ann-Katrin Grotle (University of Texas at Arlington), Jennifer Vranish (Alma College), Jody Greaney (University of Texas at Arlington), R. Brothers (University of Texas at Arlington), Paul Fadel (University of Texas at Arlington)

Background: The prevalence of hypertension (HTN) is highest in the non-Hispanic Black (BL) population. Notably, BL women have an equal or greater HTN prevalence compared to BL men; however, limited studies have included women. Heightened sympathetic nervous system reactivity has been proposed as a potential mediator of elevated HTN risk in the BL population. In this regard, our laboratory previously demonstrated exaggerated sympathetic transduction at rest in young normotensive BL men compared to their non-Hispanic white (WH) counterparts. Whether similar responses are present in BL women is not known. Furthermore, whether there are sex differences in sympathetic transduction in young BL adults remains unclear. Hypothesis: We hypothesized that BL women would exhibit elevated resting sympathetic transduction compared to WH women, and that sympathetic transduction would be comparable between BL women and men.

Methods: Six young healthy BL women (age: 20 ± 1 years), six WH women (age: 21 ± 1 years) and six BL men (age: 21 ± 1 years) were studied. Heart rate (ECG), muscle sympathetic nerve activity (MSNA; peroneal microneurography) and beat-to-beat blood pressure (BP; Finometer) were continuously measured under resting conditions for 19 ± 1 min. Sympathetic transduction was quantified as peak changes in mean arterial pressure (MAP) and the nadir of total vascular conductance (TVC) over 10 cardiac cycles following spontaneous bursts of MSNA using signal-averaging. All data are expressed as mean ± SEM.

Results: Resting BP and heart rate were not different between groups (all P gt; 0.05). Likewise, BL women had similar MSNA burst frequency (BL women: 12 ± 2 vs. WH women: 14 ± 1 bursts/min; P = 0.475) and burst incidence (BL women: 21 ± 2 vs. WH women: 24 ± 2 bursts/100 cardiac cycles; P = 0.477) compared to WH women, and BL men (13 ± 1 bursts/min, 21 ± 1 bursts/100 cardiac cycles; P = 0.539). For peak increases in MAP following MSNA bursts, there were no differences between BL and WH women (BL women: Δ+2.3 ± 0.4 vs. WH women: Δ+2.1 ± 0.2 mmHg; P = 0.741). Peak reductions in TVC were also not different in women (BL women: Δ-2.1 ± 0.3 vs. WH women Δ-2.4 ± 0.6 mL/min/mmHg; P = 0.966). However, in comparison to BL men, BL women had lower MAP (women: Δ+2.3 ± 0.4 vs. men: Δ+5.5 ± 1.1 mmHg; P = 0.011) and TVC (P = 0.036) responses.

Conclusion: Contrary to our hypothesis, these preliminary data suggest similar beat-to-beat sympathetic transduction at rest in BL and WH women. Interestingly, sympathetic transduction at rest was lower in BL women compared to BL men highlighting a potential differential effect of sex on BP regulation in young BL adults. Collectively, these findings suggest that augmented sympathetic transduction is not likely an early contributor to the greater prevalence of HTN in BL women.

This work was supported by American Heart Association Predoctoral Fellowship (Grant # 20PRE34990010, Stephens) and NIH R15 (HL156128)