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Post‐traumatic stress sensitizes the angiotensin II‐elicited hypertensive response
Author(s) -
Xue Baojian,
Yu Yang,
Wei ShunGuang,
Beltz Terry G,
Guo Fang,
Felder Robert B,
Johnson Alan Kim
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.866.2
Subject(s) - endocrinology , angiotensin ii , medicine , proinflammatory cytokine , renin–angiotensin system , amygdala , lamina terminalis , downregulation and upregulation , tumor necrosis factor alpha , inflammation , central nervous system , receptor , chemistry , blood pressure , biochemistry , gene
Post‐traumatic stress disorder (PTSD) is associated with an activated renin‐angiotensin system (RAS) and elevated levels of proinflammatory cytokines (PICs) in the circulation and in the central nervous system (CNS). Using an Induction‐Delay‐Expression experimental paradigm, our previous studies demonstrated that activation of central RAS and inflammation by various challenges sensitizes angiotensin (ANG) II‐elicited hypertension. The present study investigated whether the ANG II‐elicited hypertensive response is also sensitized in a model of PTSD. The resident‐intruder paradigm was used to model PTSD. Each intruder rat (male Sprague‐Dawley) was exposed to a different resident (male Long‐Evans) for 2 hours on three days with each session separated by 1 day. Beginning on day 3 after the last exposure, the intruder (PTSD) rats and unstressed control rats received a subcutaneous infusion of ANG II (120 ng/kg/min) for 2 weeks. The PTSD rats had a significantly enhanced hypertensive response to the ANG II infusion when compared to control rats (Δ35.9±2.5 mmHg vs. Δ17.9±3.9 mmHg). In a separate group of rats, the brains of control and PTSD rats were collected on day 3 after the last exposure to determine mRNA expression of RAS and PIC components in the lamina terminalis (LT) and the hypothalamic paraventricular nucleus (PVN). The results showed that PTSD had upregulated expression of angiotensin type 1 receptor, tumor necrosis factor‐α, interleukin (IL)‐1β and IL‐6 in the LT, but not in the PVN. These results support the hypothesis that conditions upregulating the central RAS and PICs sensitize ANG II‐induced hypertension, and suggest that disorders such as PTSD may predispose individuals to exacerbation of renin‐angiotensin‐elicited hypertension. Support or Funding Information This work was supported by the NIH grants HL‐14388 (AKJ), HL‐98207 (AKJ), HL‐096671 (RBF) HL‐073986 (RBF), with partial support from the Department of Veterans Affairs (RBF).