Posttraumatic stress disorder (PTSD) is characterized by increased sympathetic nervous system (SNS) activity, blunted parasympathetic nervous system (PNS) activity, and impaired baroreflex sensitivity (BRS), which contribute to accelerated cardiovascular disease. Patients with PTSD also have chronic stress-related elevations in resting blood pressure (BP), often in the prehypertensive range; yet, it is unclear if elevated resting blood pressure (ERBP) augments these autonomic derange-ments in PTSD. We hypothesized that compared with normotensive PTSD (N-PTSD), those with ERBP (E-PTSD) have further increased SNS, decreased PNS activity, and impaired BRS at rest and exaggerated SNS reactivity, PNS withdrawal, and pressor responses during stress. In 16 E-PTSD and 17 matched N-PTSD, we measured continuous BP, ECG, muscle sympathetic nerve activity (MSNA), and heart rate variability (HRV) markers reflecting cardiac PNS activity [stan-dard deviation of R-R intervals (SDNN), root mean square of differences in successive R-R intervals (RMSSD), and high frequency power (HF)] during 5 min of rest and 3 min of mental arithmetic. Resting MSNA (P = 0.943), sympathetic BRS (P = 0.189), and cardiovagal BRS (P = 0.332) were similar between groups. However, baseline SDNN (56 ± 6 vs. 78 ± 8 ms, P = 0.019), RMSSD (39 ± 6 vs. 63 ± 9 ms, P = 0.018), and HF (378 ± 103 vs. 693 ± 92 ms2, P = 0.015) were lower in E-PTSD versus N-PTSD. During mental stress, the systolic blood pressure response (P = 0.011) was augmented in E-PTSD. Although MSNA reactivity was not different (P > 0.05), the E-PTSD group had an exaggerated reduction in HRV during mental stress (P < 0.05). PTSD with ERBP have attenuated resting cardiac PNS activity, coupled with exaggerated BP reactivity and PNS withdrawal during stress.
|Original language||English (US)|
|Journal||American Journal of Physiology - Regulatory Integrative and Comparative Physiology|
|State||Published - Dec 2018|
Bibliographical noteFunding Information:
This work was supported by Merit Review Award Number I01CX001065 (to J. Park) from the United States Department of Veterans Affairs Clinical Sciences Research and Development Program, American Heart Association National Affiliate, Collaborative Sciences Award 15CSA24340001, National Institutes of Health R01 HL135183 (to J. Park), resources and the use of facilities at the Clinical Studies Center of the Atlanta Veteran Affairs Medical Center, the Atlanta Research and Education Foundation, National Institutes of Health training grant T32 DK-00756, Department of Veterans Affairs, Veterans Health Administration, Office of Research and Development and the Clinical Studies Center, Decatur, Georgia, the Atlanta Research and Education Foundation, University Research Council grant from Emory University, the Atlanta Clinical and Translational Science Institute supported by Public Health Service Grant UL1 RR-025008 from the Clinical and Translational Science Award program, National Institutes of Health, National Center for Research Resources.
© 2018, American Physiological Society. All rights reserved.
- Heart rate variability
- Mental stress
- Muscle sympathetic nerve activity
- Parasympathetic nervous system
- Traumatic stress disorder