The pathophysiologic mechanisms of formation endothelial dysfunction in condition of the chronic psycho-emotional stress

Abstract

The pathophysiologic mechanisms of endothelial dysfunction formation in condition of the chronic psychoemotional stress have been studied. 160 railroad engineers and 100 healthy volunteers were examined. The activity of the stress systems was measured by the level of adrenocorticotropic hormone, cortisol, corticosterone, noradrenaline in the blood. Secretory function of vascular endothelium was measured by release of nitrogen oxide and endothelin-1. The condition of antioxidant (plasma antioxidant activity) and prooxidant systems (diene conjugats), inflammatory processes (concentration of high-sensitivity C-reactive protein), the concentration of peptide hormone angiotensin-II were studied among the factors influence on endothelial function. The increasing secretion of nitrogen oxide took place in the first years of the chronic psycho-emotional stress effect against the backdrop of vasoconstrictor effects of high concentration of glucocorticoids and catecholamines. It taken place against the backdrop of the emerging oxidative stress and compensatory growth of plasma antioxidant activity. The decreasing secretion of nitrogen oxide took place after 12–15 years of the chronic psycho-emotional stress factors effects. It was accompanied by the increasing of diene conjugats and concentration of high-sensitivity C-reactive protein and decreasing of plasma antioxidant activity and endothelin-1. The significant decreasing of nitrogen oxide and plasma antioxidant activity took place after 20 years of the chronic psycho-emotional stress effects. It was promoted by the significant increase of vasoconstrictor concentration of endothelin-1 and angiotensin-II, high activity of oxidant stress and inflammation. The effect of the chronic psycho-emotional stress factors leads to the appearance of endothelial dysfunction. The endothelial dysfunction activated by the processes of oxidative stress and inflammation, high levels of endothelin-1 and angiotensin-II.

Keywords

chronic stress / endothelial dysfunction / nitrogen oxide / endothelin-1 / oxidative stress / angiotensin-II / highsensitivity C-reactive protein / plasma antioxidant activity

References

[1] Коноплева, Л.Ф. Эндотелиальная дисфункция в патогенезе сердечно-сосудистых заболеваний и методы ее коррекции

[2] / Л.Ф. Коноплева // Therapia. – 2011. – Т. 56, № 3. – С. 26–30.

[3] Barhoumi, T. Erythropoietin-induced hypertension and vascular injury in mice overexpressing human endothelin-1: Exercise attenuated hypertension, oxidative stress, inflammation and immune response / T. Barhoumi [et al.] // Journal of Hypertension. – 2014. – Vol. 32, №4. – P. 784–94.

[4] Bruder-Nascimento, T. Chronic stress improves NOand Ca2+ flux-dependent vascular function: a pharmacological study / T. Bruder-Nascimento [et al.] // Arq Bras Cardiol. – 2015. – Vol. 104, № 3. – P. 226–33.

[5] Deacon, K. Endothelin-1 (ET-1) increases the expression of remodeling genes in vascular smooth muscle through linked calcium and cAMP pathwyas: role of phospholipase A(2) (sPLA(2))/cyclooxygenase-2 (COX-2)/prostacyclin receptordependent autocrine loop / K. Deacon [et al.] // J Biol. Chem. – 2010. – Vol. 285, № 34. – P. 25913–25927.

[6] Desai, A. META060 attenuates TNF-¯activated inflammation, end othe lial -mon ocyt e i nter act ions, an d m atr ix metalloproteinase-9 expression, and inhibits NF-¯B and AP-1 in THP-1 monocytes / A. Desai [et al.] // Atherosclerosis. – 2012. – Vol. 223, № 1. – P. 130–136.

[7] Forstermann, U. Therapeutic effect of enhancing endothelial nitric oxide synthase (eNOS) expression and preventing eNOS uncoupling / U. Forstermann // Br. J. Pharmacol. – 2011. – Vol. 164, № 2. – P. 213–223.

[8] Hamer, M. Psychological distress as a risk factor for death from cerebrovascular disease / M. Hamer [et al.] // CMAJ., 2012. – Vol. 184, № 13. – P. 1461–1466.

[9] Kuo, L. Vasomotor regulation of coronary microcirculation by oxidative stress: Role of arginase / L. Kuo [et al.] // Frontiers in Immunology. – 2013. – Vol.4, Article 237. – P. 67–78.

[10] Moisan, M.P. Overview of acute and chronic stress responses / M.P. Moisan [et al.] // Med. Sci. – 2012. – Vol. 28, № 6–7. – P.

[11] 612–617.

[12] Molnar, G.A. Glucocorticoid-related signaling effects in vascular smooth muscle cells / G.A. Molnar [et al.] // Hypertension – 2008. – Vol. 51, №5. – P. 1372–1378.

[13] Montezano, A.C. Angiotensin II and vascular injury / A.C. Montezano [et al.] // Curr Hypertens Rep. – 2014. – Vol. 16, № 6. – P. 431.

[14] Poitras, V.J. The impact of acute mental stress on vascular en dothelial function: evidence, mechanisms and importance / V.J. Poitras [et al.] // Int. J. Psychophysiol. – 2013. – Vol. 88, № 2. – P. 124–135.

[15] Park, K.H. Endothelial Dysfunction: Clinical Implications in Cardiovascular Disease and Therapeutic Approaches / K.H. Park [et al.] // J. Korean Med. Sci. – 2015. – Vol. 30, № 9. – P. 1213–1225.

[16] Sankaralingam, S. Arginase contributes to endothelial cell oxidative stress in response to plasma from women with preeclampsia / S. Sankaralingam [et al.] // Cardiovascular Research. – 2010. – Vol. 85, № 1. – P. 194–203.

[17] Sun, X. Endothelin-1 induces a glycolytic switch in pulmonary arterial endothelial cells via the mitochondrial translocation of endothelial nitric oxide synthase / X. Sun [et al.] // American Journal of Respiratory Cell and Molecular Biology. – 2014. – Vol. 50, № 6. – P. 1084–1095.

[18] Veyama, T. Molekular mechanism of emotional stress-induced nd catecholamine-induced heart attacs / T. Veyama [et al.] // J. Cardiovasc. Pharmacol. – 2003. – Jan.; Suppl 1. – S. 115–118.

[19] Vita, J.A. Endothelial function / J.A. Vita // Circulation. – 2011. – Vol. 20, № 124 (25). – P. 906–912.

[20] Zhao, X.Q. CRP enhances soluble LOX-1 release from macrophages by activating TNF-¯ converting enzyme / X.Q. Zhao [et al.] // J. Lipid. Res. – 2011. – Vol. 52, № .5. – P. 923–933.