Post-traumatic stress disorder (PTSD) is a highly prevalent anxiety disorder that is associated with an increased risk of cardiovascular (CV) disease and hypertension. Given the large numbers of Veterans returning from Iraq and Afghanistan afflicted with PTSD, addressing this under-recognized but highly significant consequence of PTSD is of paramount importance. The mechanisms underlying increased CV risk in PTSD remains unknown. One potential mechanism is overactivation of the sympathetic nervous system (SNS), both at rest and during stress. Previous studies have shown that PTSD patients have higher resting heart rates and blood pressure (BP), greater cardiovascular reactivity during stress, and reduced heart rate variability, suggesting a state of heightened sympathetic activity. Although SNS hyperactivity is implicated in PTSD based on these observed indirect derangements, SNS regulation has never before been rigorously investigated in this population, and the underlying mechanisms and potential interventions targeting SNS activity and CV risk remain unexplored. The goals of this study are to determine if: 1) PTSD patients have higher resting SNS activity, and greater SNS reactivity during mental stress; 2) PTSD patients have abnormal arterial baroreflex sensitivity (BRS) that underlies SNS overactivity at baseline and during mental stress; 3) device-guided slow breathing (DGB) acutely improves SNS activity and BRS in PTSD patients; and 4) 8 weeks of daily DGB therapy improves SNS activity and hemodynamic profiles at rest and during mental stress. Furthermore, given that around half of PTSD patients have comorbid major depression (MD), and MD is independently associated with CV risk and SNS dysregulation, we hypothesize that comorbid MD augments SNS reactivity at rest and during mental stress in PTSD patients. To achieve these goals, we will measure sympathetic nerve activity directly using microneurography in young, prehypertensive veterans with PTSD (with and without MD) compared to non-PTSD controls (with and without MD) at rest and during mental stress, perform arterial baroreflex testing using the modified Oxford technique, and perform an 8-week pilot trial on the benefits of DGB on SNS reactivity and regulation. We hypothesize that PTSD patients have greater SNS activity at baseline and greater SNS reactivity during sympathoexcitation with mental stress, both related to combat recall and other forms of mental stress. We expect that these derangements are independent of MD, but that comorbid MD augments SNS reactivity in PTSD. We further propose that SNS overactivity is mediated by arterial baroreflex dysfunction at rest and during mental stress. Finally, previous studies have shown that device guided slow breathing (DGB), in which breathing is slowed to subphysiologic rates (of 5-6 breaths/minute) via an interactive biofeedback device, reduces BP, SNS activity, and improves BRS in patients with hypertension. DGB has never previously been tested in PTSD and may be a novel nonpharmacologic approach to reducing SNS activity and restoring BRS in these patients. We hypothesize that DGB acutely improves SNS overactivity, BP, and BRS, and chronically leads to sustained reductions in SNS and BRS at rest and during stress, in prehypertensive patients with PTSD. Improving SNS overactivity and BRS may have long term benefits on reducing CV risk in PTSD patients.