Why the study?
Longitudinal assessments of MSNA in pregnancy are scarce and have primarily focused on resting burst frequency, leaving the impact of normal pregnancy on burst amplitude distributions and responses to orthostatic stress unclear.
Does normal pregnancy alter sympathetic neural burst frequency and amplitude in response to orthostatic stress in healthy women?
Does normal pregnancy alter sympathetic neural burst frequency and amplitude in response to orthostatic stress in healthy women?
Normal pregnancy attenuates orthostatically induced increases in sympathetic nerve activity burst frequency and amplitude, which may serve as a natural adaptation to prevent sympathetic hyper-reactivity.
Late pregnancy attenuates sympathetic responses to orthostasis; hypothesis-generating for mechanisms of orthostatic tolerance and hypertensive disorders.
Sympathetic activation is a hallmark of pregnancy. However, longitudinal assessments of muscle sympathetic nerve activity (MSNA) in pregnancy are scarce and have primarily focused on burst occurrence (frequency) at rest, despite burst strength (amplitude) representing distinct characteristics of sympathetic outflow. Thus, we assessed MSNA burst amplitude distributions in healthy women to determine the impact of normal pregnancy on neural discharge patterns in response to orthostatic stress. Twenty-six women were studied longitudinally during pre-, early- (4–8 wk of gestation), and late (32–36 wk) pregnancy, as well as postpartum (6–10 wk after delivery). MSNA, blood pressure (BP), and heart rate (HR) were measured in the supine posture and during graded head-up tilt (30° and 60° HUT). Mean and median MSNA burst amplitudes were used to characterize burst amplitude distribution. In late pregnancy, women demonstrated smaller increases in HR ( P < 0.001) during 60° HUT and larger increases in systolic BP ( P = 0.043) throughout orthostasis, compared with prepregnancy. The increase in MSNA burst frequency during late- relative to prepregnancy (Late: Δ14[10] vs. Pre: Δ21[9] bursts/min; P = 0.001) was smaller during 60° HUT, whereas increases in burst incidence were smaller in late- relative to prepregnancy throughout orthostasis ( P = 0.009). Nonetheless, median burst amplitude was smaller throughout orthostasis in late compared with prepregnancy ( P = 0.038). Thus, while supine MSNA burst frequency was greater in late pregnancy, increases in burst frequency and strength during orthostasis were attenuated. These smaller, orthostatically induced MSNA increases may reflect natural adaptions of pregnancy serving to prevent sympathetic hyper-reactivity that is common in pathological states.
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D’Souza et al. (2022) studied this question.
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