Abstract
Recently, we reported that muscle sympathetic nerve activity (MSNA) is not predictive of vascular nor blood pressure outcomes during the cold pressor test (CPT) in young healthy females. Instead, we observed substantial variability in vascular responses to the CPT which ranged widely from decreases in blood flow and vascular conductance to increases in these same outcomes. Interindividual differences in circulating reproductive hormones may account for this female-specific variability in vascular responses to acute elevations in MSNA. Therefore, the purpose of this study was to test the hypothesis that reproductive hormones account for variability in MSNA, femoral blood flow (FBF), and femoral vascular conductance (FVC) during the CPT in females. We retrospectively assessed data from 9 young healthy females (age: 24±3 years) in the low hormone phase of their menstrual cycle (days 1-5). Intravenous blood samples were obtained and prospectively analyzed to assess concentrations of circulating reproductive hormones (radioimmunoassay). Integrated peroneal MSNA (microneurography; NeuroAmpEX, ADI) was quantified at rest and during a 3-minute hand CPT. Mean arterial pressure (MAP) was measured beat-by-beat (Finometer Midi, FMS) and duplex vascular ultrasound was used to measure FBF; FVC was quantified as FBF/MAP (mL/min/mmHg). All variables are expressed as the difference between the average CPT value and the average baseline value. CPT-induced changes in MSNA burst incidence (bursts/100hb) were not related to [17-beta-estradiol] (R2=0.05; P=0.60), [progesterone] (R2=0.11, P=0.47), or [free testosterone] (R2=0.01, P=0.81). Similarly, changes in FBF and FVC were not related to [17-beta-estradiol] (FBF: R2=0.04, P=0.67; FVC: R2=0.01, P=0.80) or [progesterone] (FBF: R2=0.04, P=0.67; FVC: R2=0.09, P=0.51). However, there was a negative correlation between [free testosterone] and the changes in both FBF (R2=0.69, P=0.02) and FVC (R2=0.66, P=0.03). In other words, females with higher free testosterone demonstrated larger decreases in FBF and FVC during the CPT relative to those with lower free testosterone concentrations. These data suggest that circulating free testosterone may act to increase the vasoconstrictive consequences of MSNA in females, and may account for the previously observed variability in vascular responses to MSNA during acute stress. This project was funded by: NSERC and FRQ-S. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
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