The Association of Psychological Stress Related Cytokines (TNF Alpha, IFN-Gamma) with Essential Hypertension in Ningxia Hui Autonomous Region

DOI: 10.4236/ojemd.2013.37038   PDF   HTML     2,495 Downloads   4,352 Views   Citations


The study aimed to explore the association between psychological stress-related cytokines and essential hypertension to provide the theoretical basis for the prevention and control of the essential hypertension. We screened hypertension patients in six communities in Wuzhong City of Ningxia, and chose the healthy people who had lived in the same community for full 5 years as a control group. Finally, we selected 210 pairs of cases and controls randomly, including 108 pairs of Hui and 102 pairs of Han (50% male; age 35 -74). The results showed that the serum TNF alpha levels of hypertension group were higher than the control group (ρ < 0.01), and the serum IFN-gamma levels were lower than the control group both in Hui and Han (ρ < 0.01). Further analysis showed that the serum TNF alpha level of the Hui hypertension group was higher than the Han hypertension group (ρ < 0.01), while the serum IFN-gamma level was lower than Han hypertension group (ρ < 0.01). In conclusion, TNF alpha and IFN-gamma were the important related cytokines between psychological stress and hypertension, and taking effective measures to control the level of serum TNF alpha. IFN-gamma may have the vital significance in alleviating or preventing the genesis and development of essential hypertension.

Share and Cite:

Z. Niu, J. Zhou, W. Ji, H. Li, D. Bai and H. Yang, "The Association of Psychological Stress Related Cytokines (TNF Alpha, IFN-Gamma) with Essential Hypertension in Ningxia Hui Autonomous Region," Open Journal of Endocrine and Metabolic Diseases, Vol. 3 No. 7, 2013, pp. 276-282. doi: 10.4236/ojemd.2013.37038.

Conflicts of Interest

The authors declare no conflicts of interest.


[1] J. A. Staessen, J.-G. Wang and L. Thijs, “Cardiovascular Prevention and Blood Pressure Reduction: A Quantitative Overview Updated until March 2003,” Journal of Human Hypertension, Vol. 21, No. 6, 2003, pp. 1055-1076.
[2] M. K. Patricia, W. Megan, R. Kristi, K. W. Paul and H. Jiang, “Worldwide Prevalence of Hypertension: A Systematic Review,” Journal of Hypertension, Vol. 22, No. 1, 2004, pp. 11-19.
[3] M. K. Patricia, W. Megan, R. Kristi, M. Paul, K. W. Paul and H. Jiang, “Global Burden of Hypertension: Analysis of Worldwide Data,” The Lancet, Vol. 365, No. 9455, 2005, pp. 217-223.
[4] S. Krisela, A. G. Thomas, B. Debbie, L. Ria and F. Jean, “Hypertension in South African Adults: Results from the Demographic and Health Survey, 1998,” Journal of Hypertension, Vol. 19, No. 10, 2001, pp. 1717-1725.
[5] J. Wang, X. Ning, L. Yang, H. Lu, J. Tu and W. Jin, “Trends of Hypertension Prevalence, Awareness, Treatment and Control in Rural Areas of Northern China during 1991-2011,” Journal of Human Hypertension, 2013.
[6] Y. Gao, G. Chen, H. Tian, L. Lin, J. Lu, J. P. Weng, et al., “Prevalence of Hypertension in China: A Cross-Sectional Study,” Plos One, Vol. 8, No. 6, 2013, p. e65938.
[7] T. M. Spruill, “Chronic Psychosocial Stress and Hypertension,” Current Hypertension Reports, Vol. 12, No. 1, 2010, pp. 10-16.
[8] R. M. Osti, G. Trombini and B. Magnani, “Stress and Distress in Essential Hypertension,” Psychotherapy and Psychosomatics, Vol. 33, No. 4, 1980, pp. 193-197.
[9] T. Okura, M. Jotoku, J. Irita, D. Enomoto, T. Nagao, V. R. Desilva, et al., “Association between Cystatin C and Inflammation in Patients with Essential Hypertension,” Clinical and Experimental Nephrology, Vol. 14, No. 6, 2010, pp. 584-588.
[10] B. Chamarthi, G. H. Williams, V. Ricchiuti, N. Srikumar, P. N. Hopkins, J. M. Luther, et al., “Inflammation and Hypertension: The Interplay of Interleukin-6, Dietary Sodium, and the Renin-Angiotensin System in Humans,” American Journal of Hypertension, Vol. 24, No. 10, 2011, pp. 1143-1148.
[11] M. Hamer and A. Stepton, “Association between Physical Fitness, Parasympathetic Control and Proinflammatory Responses to Mental Stress,” Psychosomatic Medicine, Vol. 69, No. 7, 2007, pp. 660-666.
[12] S. C. Harwani, M. W. Chapleau, K. L. Legge, Z. K. Ballas and F. M. Abboud, “Neurohormonal Modulation of the Innate Immune System Is Proinflammatory in the Prehypertensive Spontaneously Hypertensive Rat, a Genetic Model of Essential Hypertension,” Circulation Research, Vol. 111, No. 9, 2012, pp. 1190-1197.
[13] S. Sriramula, J. P. Cardinale and J. Francis, “Inhibition of TNF in the Brain Reverses Alterations in RAS Components and Attenuates Angiotensin II-Induced Hypertension,” Plos One, Vol. 8, No. 5, 2013, p. e63847.
[14] W. Rief and M. Fichter, “The Symptom Check List SCL-90-Rand and Its Ability to Discriminate between Dysthymia, Anxiety Disorders, and Anorexia Nervosa,” Psychopathology, Vol. 25, No. 3, 1992, pp. 128-138.
[15] W. W. Ji, J. Zhou, H. X. Li, D. Bai and H. F. Yang, “Psycho-Behavioral Status and Influencing Factors in Hui and Han Chinese Patients with Hypertension,” Occupational and Environmental Medicine, Vol. 29, No. 2, 2012, pp. 104-106.
[16] A. Grimsrud, D. J. Stein, S. Seedat, D. Williams and L. Myer, “The Association between Hypertension and Depression and Anxiety Disorders: Results from a NationallyRepresentative Sample of South African Adults,” Plos One, Vol. 4, No. 5, 2009, p. e5552.
[17] J. E. Dimsdale, “Psychological Stress and Cardiovascular Disease,” Journal of the American College of Cardiology, Vol. 51, No. 13, 2008, pp. 1237-1246.
[18] M. Domanski and M. Proschan, “The Metabolic Syndrome,” Journal of the American College of Cardiology, Vol. 43, 2004, pp. 138-139.
[19] S. S. David, B. C. Janet, A. J. Sherman, L. K. Nora, R. B. Steven, M. G. Joanne, et al., “Social Support, Stress and Blood Pressure in Black Adults,” Epidemiology, Vol. 8, No. 5, 1997, pp. 482-497.
[20] J. E. Williams, F. J. Nieto, C. P. Sanford and H. A. Tyroler, “Effects of an Angry Temperament on Coronary Heart Disease Risk: The Atherosclerosis Risk in Communities Study,” American Journal of Epidemiology, Vol. 154, No. 3, 2001, pp. 230-235.
[21] A. Appels, F. Bär, J. Bär, C. Bruggeman and M. D. Baets, “Inflammation, Depressive Symptomatology, and Coronary Artery Disease,” Psychosomatic Medicine, Vol. 62, No. 5, 2000, pp. 601-605.
[22] J. P. Granger, B. T. Alexander, M. T. Llinas, W. A. Bennett and R. A. Khalil, “Pathophysiology of Hypertension during Preeclampsia Linking Placental Ischemia with Endothelial Dysfunction,” Hypertension, Vol. 38, No. 3, 2001, pp. 718-722.
[23] L. E. Bautista, L. M. Vera, I. A. Arenas and G. Gamarra, “Independent Association between Inflammatory Markers (C-Reactive Protein, Interleukin-6, and TNF-Alpha) and Essential Hypertension,” Journal of Human Hypertension, Vol. 19, No. 2, 2004, pp. 149-157.
[24] J. L. Cheng, A. L. Wang and J. Wan, “Association between the M235T Polymorphism of the AGT Gene and Cytokines in Patients with Hypertension,” Experimental and Therapeutic Medicine, Vol. 3, No. 3, 2012, pp. 509-512.
[25] K. Matsubara, E. Abe, H. Ochi, Y. Kusanagi and M. Ito, “Changes in Concentrations of Tumor Necrosis Factor Alpha and Adhesion Molecules in Normal Pregnant Women and Those with Pregnancy-Induced Hypertension,” Journal of Obstetrics and Gynaecology Research, Vol. 29, No. 6, 2003, pp. 422-442.

comments powered by Disqus

Copyright © 2020 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.