Session: 757 APS Thermal stress, thermoregulation, and hydration Poster Session
(757.27) Estradiol Augments Sensory Nerve-Mediated Vasodilation in Young Women
Monday, April 4, 2022
10:15 AM – 12:15 PM
Location: Exhibit/Poster Hall A-B - Pennsylvania Convention Center
Poster Board Number: E476
Allyson Schwab (University of Delaware), Angelica Del Vecchio (University of Delaware), Laura Welti (University of Delaware), Katherine Haigh (University of Delaware), Ronald Feinberg (Reproductive Associates of Delaware), Shane McGinty (University of Delaware), Brett Wong (Georgia State University), Megan Wenner (University of Delaware)
Local heating of the skin elicits biphasic vasodilation: a sensory nerve-mediated initial peak (axon reflex) and an endothelial-dependent plateau. We have previously shown that sex hormones, particularly estradiol (E2), improves cutaneous endothelial-dependent vasodilation, but less is known about the effects of E2 on cutaneous sensory nerve-mediated vasodilation.
Purpose: We tested the hypothesis that E2 enhances sensory-nerve mediated vasodilation in response to local heating of the skin in young women.
Methods: We retrospectively analyzed data in 15 healthy young women (age 24 ± 4 yr; MAP 84 ± 6 mmHg; BMI 24 ± 3 kg/m2). Endogenous sex hormone production was suppressed with daily administration of a gonadotropin-releasing hormone antagonist (GnRHant; Ganirelix) for 10 days. E2 (0.1 mg/day, Vivelle-Dot) was added back via transdermal patch on days 4–10. Cutaneous vasodilatory responses to local heating were measured on days 4 and 10 using laser Doppler flowmetry during microdialysis perfusions of lactated Ringer’s (control), and in a subset of women (n=6), L-NAME (non-selective nitric oxide synthase inhibition). Cutaneous vascular conductance (CVC) was calculated during the initial peak of the axon reflex during local heating (42°C) and normalized to maximal vasodilation achieved by perfusion of sodium nitroprusside (28mM) and heating to 43°C.
Results: Sensory nerve-mediated vasodilation increased during E2 administration compared to GnRHant (E2: 71 ± 15, GnRHant: 57 ± 18 %CVCmax; p=0.046). Blockade of nitric oxide with L-NAME did not blunt the axon reflex during GnRHant (control: 57 ± 18 vs. L-NAME: 50 ± 17 %CVCmax; p=0.401) or E2 administration (control: 71 ± 15 vs. L-NAME: 52 ± 19 %CVCmax; p=0.152).
Conclusion: These preliminary findings suggest that E2 enhances sensory nerve-mediated vasodilation in young women, and that this may occur through mechanisms independent of nitric oxide. Future mechanistic studies isolating the nitric oxide component and other pathways could help elucidate the role of E2 in sensory nerve-mediated vasodilation.
