Contribution of neurohumoral dysfunction and overweight to the course of essential hypertension
- Authors: Bunova SS, Bunova SS
- Issue: Vol 81, No 5 (2009)
- Pages: 71-74
- Section: Editorial
- URL: https://journals.rcsi.science/0040-3660/article/view/30368
- ID: 30368
Cite item
Full Text
Abstract
Aim. To determine the role of neurohumoral dysfunction and overweight in a clinical course of arterial hypertension (AH).
Material and methods. 200 participants of the study aged 30-60 years with AH degree I-II with low, moderate and high overall cardiovascular risk and mean disease duration 11.1 ± 9.5 years were examined for body mass index, levels of leptin, soluble leptin receptor, insulin, serotonin and adrenoreactivity.
Results. Neurohumoral dysfunction correlated with body mass index. It manifested with elevation of insulin and leptin levels, sympathetic hyperactivity and a decrease of serotonin.
Conclusion. One of the mechanisms forming and sustaining AH in patients with overweight is leptin-dependent sympathetic hyperactivity while serotonin system activation is more important for patients with normal body weight. Hypertensive patients with obesity demonstrate insulin-dependent hyperleptinemia.
Material and methods. 200 participants of the study aged 30-60 years with AH degree I-II with low, moderate and high overall cardiovascular risk and mean disease duration 11.1 ± 9.5 years were examined for body mass index, levels of leptin, soluble leptin receptor, insulin, serotonin and adrenoreactivity.
Results. Neurohumoral dysfunction correlated with body mass index. It manifested with elevation of insulin and leptin levels, sympathetic hyperactivity and a decrease of serotonin.
Conclusion. One of the mechanisms forming and sustaining AH in patients with overweight is leptin-dependent sympathetic hyperactivity while serotonin system activation is more important for patients with normal body weight. Hypertensive patients with obesity demonstrate insulin-dependent hyperleptinemia.
References
- Оганов Р. Г. Профилактика сердечно-сосудистых заболеваний: возможности практического здравоохранения. Кардиоваск. тер. и профилакт. 2002; 1: 5-9.
- Шальнова С. А, Деев А. Д., Оганов Р. Г. и др. Роль систолического и диастолического артериального давления для прогноза смертности от сердечно-сосудистых заболеваний. Кардиоваск. тер. и профилакт. 2002; 1: 10-15.
- Оганов Р. Г. Эпидемиология артериальной гипертонии в России и возможности профилактики. Тер. арх. 1999; 69(8): 66-69.
- Стрюк Р. И., Длусская И. Г. Адренореактивность и сердечно-сосудистая система. М.; 2003.
- Burns K. D. Angiotensin II and its receptor in the diabetic kidney. Am. J. Kidney Dis. 2000; 36(3): 446-467.
- Kagan B. L. et al. Elevated lipid levels in vietnam veterans with chronic posttaumatic stress disorder. Biol. Psychiatry 1999; 45(3): 374-377.
- Felber J. P. et al. Insulin and blood pressure in the obesity. Diabetologia 1995; 1: 1220-1228.
- Зарецкий Д. В., Каленникова Е. И., Ливанова Л. М. и др. Активность моноаминергических систем гипоталамуса крыс при остром иммобилизационном стрессе после хронического стрессирования. Журн. высш. нервн. деят. 1999; 49(2): 313-320.
- Симоненков А. П., Федоров В. Д., Федоров А. В. и др. Способность гемоглобина и миоглобина вызывать спазм гладкой мускулатуры и ускорять разрушение тромбоцитов. Описание серотонинферропротеиновых рецепторов. Вестн. РАМН. 1995; 12: 45-51.
- Симоненков А. П., Федоров В. Д. О единстве тканевой гипоксии и шока. Анестезиол. и реаниматол. 2001; 6: 73-76.
- Симоненков А. П., Федоров В. Д. Серотонин в генезе стресса и адаптации. Вестн. РАМН. 2002; 8: 9-13.
- Tentolouris N. et al. Sympathetic system activity in obesity and metabolic syndrome. Ann. N. Y. Acad. Sci. 2006; 1083: 129-152.
- Weidmann P. et al. Association between sympathetic activity and the atherogenic serum cholesterol fraction. J. Mol. Med. 1990; 68(5): 269-276.
- Kannel W. B. et al. Higgis regional obesity and risk of cardiovascular disease; the Framingham study. J. Clin. Epidemiol. 1991; 44(2): 183-190.
- Julius S. Changing role of the autonomic nervous system in human hypertension. J. Hypertens. 1990; 8: 59-65.
- Es1er M. Sympathetic activity in experimental and human hypertension. In: Mancia G., ed. Handbook of hypertension. Amsterdam: Elsevier; 1997; vol. 17: 628-673.
- Чазова И. Е., Мычка В. Б. Метаболический синдром. М.: Изд-во "Медиа Медика"; 2004.
- Dagogo-Jack A. et al. Plasma leptin and insulin relationships in obese and nonobese humans. Diabetes 1998; 45: 695-698.
- Kuczmarski R. J. et al. Increasing prevalence of overweight among US adults. The National Health and Nutrition Examination Surveys, 1960 to 1991. J. A. M. A. 1994; 272: 205-211.
- Шпак Л. В., Колбасников С. В. Выраженность тревожных расстройств и состояние кровообращения у больных гипертонической болезнью. Тер. арх. 1998; 6: 50-53.
- Phillips M. S. et al. Leptin receptor missense mutation in the fatty Zuckerrat. Nat. Genet. 1996; 13: 18-19.
- Vanhala M. G. et al. Metabolic syndrome in middle-aged Finnish population. J. Cardiovasc. Risk 1997; 4: 291-295.
- Maffei M. et al. Leptin levels in human and rodent: measurement of plasma leptin and ob RNA in obese and weight-reduced subjects. Nat. Med. 1995; 1: 1155-1161.
- Балаболкин М. И., Дедов И. И. Генетические аспекты сахарного диабета. Сахар. диабет. 2000; 1: 2-10.
- Sonnenberg G. E. et al. A novel pathway to the manifestation of metabolic syndrome. Obes. Res. 2004; 12(2): 180-192.
- Bjorntorp P. Obesity. Lancet. 1997; 350: 423-426.
- Blum W. F. et al. Plasma leptin levels in healthy children and adolescents: dependence on body mass index, body fat mass, gender, pubertal stage, and testosterone. J. Clin. Endocrinol. 1997; 82: 2904-2910.
- Saab P. G. et al. Cardiovascular responsibility to stress in adolescents with and without persistently elevated blood pressure. J. Hypertens. 2001; 19: 21-27.
- Eikelis N. et al. Extraadipocyte leptin release in human obesity and its relation to sympathoadrenal function. Am. J. Physiol. Endocrinol. Metab. 2004; 286: 744-752.
![](/img/style/loading.gif)