Posttraumatic Stress Disorder Disturbs Coronary Tone and Its Regulatory Mechanisms
- PMID: 28676988
- PMCID: PMC11481920
- DOI: 10.1007/s10571-017-0517-x
Posttraumatic Stress Disorder Disturbs Coronary Tone and Its Regulatory Mechanisms
Erratum in
-
Correction to: Posttraumatic Stress Disorder Disturbs Coronary Tone and Its Regulatory Mechanisms.Cell Mol Neurobiol. 2018 Nov;38(8):1565. doi: 10.1007/s10571-018-0619-0. Cell Mol Neurobiol. 2018. PMID: 30206749 Free PMC article.
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.
Conflict of interest statement
The authors declare that they have no conflict of interest.
Figures


Similar articles
-
Endotoxin releases a substance from the aorta that dilates an isolated arteriole by up-regulating INOS.J Surg Res. 2005 Aug;127(2):106-11. doi: 10.1016/j.jss.2005.03.025. J Surg Res. 2005. PMID: 15921695
-
Selective modulation of endogenous nitric oxide formation in ischemia/reperfusion injury in isolated rat hearts--effects on regional myocardial flow and enzyme release.Basic Res Cardiol. 2003 May;98(3):165-74. doi: 10.1007/s00395-003-0408-9. Basic Res Cardiol. 2003. PMID: 12883834
-
Voltage-dependent K+ channels regulate the duration of reactive hyperemia in the canine coronary circulation.Am J Physiol Heart Circ Physiol. 2008 May;294(5):H2371-81. doi: 10.1152/ajpheart.01279.2007. Epub 2008 Mar 28. Am J Physiol Heart Circ Physiol. 2008. PMID: 18375717
-
Inhibition of nitric oxide synthesis by NG-nitro-L-arginine methyl ester (L-NAME): requirement for bioactivation to the free acid, NG-nitro-L-arginine.Br J Pharmacol. 1996 Jul;118(6):1433-40. doi: 10.1111/j.1476-5381.1996.tb15557.x. Br J Pharmacol. 1996. PMID: 8832069 Free PMC article.
-
Aging-induced phenotypic changes and oxidative stress impair coronary arteriolar function.Circ Res. 2002 Jun 14;90(11):1159-66. doi: 10.1161/01.res.0000020401.61826.ea. Circ Res. 2002. PMID: 12065318
Cited by
-
Physical Fatigue and Morphofunctional State of the Myocardium in Experimental Chronic Stress.Dokl Biol Sci. 2019 Mar;485(1):30-32. doi: 10.1134/S0012496619020042. Epub 2019 Jun 13. Dokl Biol Sci. 2019. PMID: 31197589
-
Unraveling the Liver-Brain Axis: Resveratrol's Modulation of Key Enzymes in Stress-Related Anxiety.Biomedicines. 2024 Sep 10;12(9):2063. doi: 10.3390/biomedicines12092063. Biomedicines. 2024. PMID: 39335576 Free PMC article.
-
Mechanisms of Susceptibility and Resilience to PTSD: Role of Dopamine Metabolism and BDNF Expression in the Hippocampus.Int J Mol Sci. 2022 Nov 23;23(23):14575. doi: 10.3390/ijms232314575. Int J Mol Sci. 2022. PMID: 36498900 Free PMC article.
-
Cerebral Blood Flow in Predator Stress-Resilient and -Susceptible Rats and Mechanisms of Resilience.Int J Mol Sci. 2022 Nov 25;23(23):14729. doi: 10.3390/ijms232314729. Int J Mol Sci. 2022. PMID: 36499055 Free PMC article.
-
Common pathways and communication between the brain and heart: connecting post-traumatic stress disorder and heart failure.Stress. 2019 Sep;22(5):530-547. doi: 10.1080/10253890.2019.1621283. Epub 2019 Jun 4. Stress. 2019. PMID: 31161843 Free PMC article. Review.
References
-
- Baker DG, Ekhator NN, Kasckow JW, Hill KK, Zoumakis E, Dashevsky BA, Chrousos GP, Geracioti TD Jr (2001) Plasma and cerebrospinal fluid Interleukin-6 concentrations in posttraumatic stress disorder. Neuroimmunomodulation 9(4):209–217 - PubMed
-
- Bryan NS, Bian K, Murad F (2009) Discovery of the nitric oxide signaling pathway and targets for drug development. Front Biosci 14:1–18 - PubMed
-
- Carda AP, Marchi KC, Rizzi E, Mecawi AS, Antunes-RJ Padovan CM, Tirapelli CR (2015) Acute restraint stress induces endothelial dysfunction: role of vasoconstrictor prostanoids and oxidative stress. Stress 18(2):233–243. doi:10.3109/10253890.2015.1014790Epub 2015 Feb 18 - PubMed
-
- Cohen H, Zohar J (2004) Animal models of post traumatic stress disorder: the use of cut off behavioral criteria. Ann N Y Acad Sci 1032:167–178 - PubMed
-
- Cohen H, Zohar J, Gidron Y, Matar MA, Belkind D, Loewenthal U, Kozlovsky N, Kaplan Z (2006) Blunted HPA axis response to stress influences susceptibility to posttraumatic stress response in rats. Biol Psychiatry 12:1208–1218 - PubMed
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical
Research Materials