Citation

Lazuko SS, Kuzhel OP, Belyaeva LE, Manukhina EB, Fred Downey H, Tseilikman OB, Komelkova MV, Tseilikman VE. Cell. Mol. Neurobiol. 2018; 38(1): 209-217.

Affiliation

South Ural State University Biomedical School, Lenin Ave, Chelyabinsk, 454080, Russian Federation. vadimed@yandex.ru.

Copyright

(Copyright © 2018, Holtzbrinck Springer Nature Publishing Group)

DOI

10.1007/s10571-017-0517-x

PMID

28676988

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.

Language: en

Keywords

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