Vasomotor symptoms of menopause, sympathetic activity, and blood pressure in postmenopausal females

Although 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 with age-matched females without VMS. Participants were grouped based on whether they currently or previously experienced VMS (n ¼ 43) or never experienced VMS (non-VMS; n ¼ 26). Heart rate (HR: electrocardiography), BP (finger plethysmography), and MSNA (microneurography) were recorded during a 10-min rest, a 2-min cold pressor test (CPT), and a 5-min recovery. Although 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/100 heartbeats, P < 0.01) was greater in the VMS group. Resting HR was lower in the VMS group (58 ± 10 vs. 62 ± 9 beats/min, P ¼ 0.04), and the standard deviation of the RR-interval HR variability (52 ± 21 vs. 38 ± 16 ms, P < 0.01), total cardiovagal baroreflex (cBRS; 12 ± 6 vs. 9 ± 3 ms/mmHg, P ¼ 0.02), and cBRS down (cBRSdown; 12 ± 6 vs. 9 ± 4 ms/mmHg, P ¼ 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). 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 with the non-VMS group. Future work on this paradoxical finding appears warranted.