Abstract
Post-traumatic stress disorder (PTSD) is a debilitating psychological disorder that increases sympathoexcitation, norepinephrine (NE) outflow, and the risk of comorbid diseases such as hypertension by >50%, but the mechanisms remain unclear. Hypertension is regulated in part due to inflammation, and our laboratory previously reported that exposure to NE can modulate levels of T-lymphocyte pro-inflammatory cytokines by redox signaling mechanisms. Therefore, we hypothesized that psychological stress-induced sympathoexcitation leads to a redox-regulated increase in pro-inflammatory cytokine production from T-lymphocytes, which impacts the development of hypertension. Utilizing a mouse-model of PTSD-like psychological stress, increased sympathoexcitation was confirmed by a 2.5 fold increase in splenic NE and 4.1 fold increase in tyrosine hydroxylase content (TH; p
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