Resting sympathetic transduction in veterans with PTSD

Posttraumatic stress disorder (PTSD) is associated with autonomic dysregulation characterized by heightened sympathetic nervous system and reduced parasympathetic nervous system activity that contribute to increased cardiovascular risk. Prior work has shown that individuals with PTSD have augmented increases in muscle sympathetic nerve activity (MSNA) during sympathoexcitatory stressors and increased vascular alpha-1 adrenergic receptor sensitivity. However, sympathetic transduction, defined as the blood pressure (BP) response to MSNA, has not been previously examined in PTSD. We investigated whether resting sympathetic transduction is increased in combat veterans with PTSD.

In 18 veterans with PTSD and 10 age-matched controls, beat-to-beat blood pressure (finger photoplethysmography), heart rate (electrocardiography), and MSNA (microneurography) were recorded at rest for 10 min. Sympathetic BP transduction was quantified using signal averaging, whereby the BP response to each MSNA burst was tracked over 15 cardiac cycles and averaged to derive the peak change in BP.

Baseline characteristics, resting MSNA, BP, and heart rate were similar between groups. Sympathetic transduction did not differ between veterans with PTSD and controls (1.16 ± 0.74 vs 1.04 ± 0.67 mmHg; p = 0.67). In the PTSD group, resting MSNA was inversely associated with sympathetic transduction (r = - 0.494, p = 0.037). No associations were found with PTSD symptom severity or psychiatric comorbidities and sympathetic transduction.

These findings suggest that resting sympathetic transduction is not altered in veterans with PTSD.