Participants with vasomotor symptoms show similar blood pressure and sympathetic activity, suggesting unique cardiovascular responses.
Objectives: While evidence suggests an association between vasomotor symptoms (VMS; hot flushes and night sweats) and elevated blood pressure (BP), it remains unknown whether females who experience VMS have elevated muscle sympathetic nerve activity (MSNA), a major modulator of BP. We hypothesized that postmenopausal females with VMS would have elevated BP and MSNA at rest and during stress compared to age-matched females without VMS. Methods: Participants were grouped based on whether they currently or previously experienced VMS (n=43) or never experienced VMS (non-VMS; n=26). Heart rate (HR: electrocardiography), BP (finger plethysmography) and MSNA (microneurography), were recorded during a 10-min rest, a two-min cold pressor test (CPT) and a five-min recovery. Results: While there were no group differences in resting mean arterial pressure (MAP) or MSNA burst frequency (p>0.05), MSNA burst incidence (53±13 vs. 44±9 bursts/100heartbeats, p<0.01) was greater in the VMS group. Resting HR was lower in the VMS group (58±10 vs. 62±9bpm; p=0.04), and the standard deviation of the RR-interval HR variability (HRV) (52±21 vs. 38±16ms, p<0.01), total cardiovagal baroreflex (cBRS;12±6 vs. 9±3ms/mmHg, p=0.02) and cBRS down (cBRSdown; 12±6 vs. 9±4ms/mmHg, p=0.01) calculated via the sequence method were greater than the non-VMS group. HR, MAP, and MSNA responsiveness to CPT were not different between groups (p>0.05). Conclusion: Contrary to our initial hypothesis, postmenopausal females with current or prior VMS demonstrated similar BP and MSNA burst frequency, with greater cardiovagal modulation and baroreflex sensitivity compared to the non-VMS group. Future work into this paradoxical finding appears warranted.
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Stokes et al. (2025) studied this question.
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