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. 2018 Jan;38(1):209-217.
doi: 10.1007/s10571-017-0517-x. Epub 2017 Jul 4.

Posttraumatic Stress Disorder Disturbs Coronary Tone and Its Regulatory Mechanisms

Affiliations

Posttraumatic Stress Disorder Disturbs Coronary Tone and Its Regulatory Mechanisms

Svetlana S Lazuko et al. Cell Mol Neurobiol. 2018 Jan.

Erratum in

Abstract

Posttraumatic stress disorder (PTSD) is associated with myocardial injury, but changes in coronary regulatory mechanisms in PTSD have not been investigated. This study evaluated the effect of PTSD-inducing stress on coronary tone and its regulation by nitric oxide (NO) and voltage-gated K+ channels. PTSD was induced by exposing rats to predator stress, 15 min daily for 10 days, followed by 14 stress-free days. Presence of PTSD was confirmed by the elevated plus-maze test. Coronary tone was evaluated from changes in coronary perfusion pressure of Langendorff isolated hearts. Predator stress induced significant decreases in coronary tone of isolated hearts and in blood pressure of intact rats. L-NAME, a non-selective NO synthase (NOS) inhibitor, but not S-MT, a selective iNOS inhibitor, and increased coronary tone of control rats. In PTSD rats, both L-NAME and S-MT increased coronary tone. Therefore, the stress-induced coronary vasodilation resulted from NO overproduction by both iNOS and eNOS. NOS induction was apparently due to systemic inflammation as evidenced by increased serum interleukin-1β and C-reactive protein in PTSD rats. Decreased corticosterone in PTSD rats may have contributed to inflammation and its effect on coronary tone. PTSD was also associated with voltage-gated K+ channel dysfunction, which would have also reduced coronary tone.

Keywords: C-reactive protein; Coronary tone; Corticosterone; Interleukin-1β; NO synthase; Posttraumatic stress disorder.

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Conflict of interest statement

The authors declare that they have no conflict of interest.

Figures

Fig. 1
Fig. 1
Effect of the non-selective NOS inhibitor, L-NAME, and the selective iNOS inhibitor, S-MT, on PTSD-associated changes in coronary perfusion pressure (CPP) of isolated hearts perfused at constant flow. *Significantly different from control, p < 0.05. #Significantly different from PTSD, p < 0.05
Fig. 2
Fig. 2
Effect of the Kv channel selective inhibitor, 4-AP, on PTSD-associated changes in coronary perfusion pressure (CPP) of isolated hearts perfused at constant flow. *Significantly different from control, p < 0.05. #Significantly different from PTSD, p < 0.05

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