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Chronic Stress in the Development of Essential Hypertension, Role of Rilmenidine in the Treatment of Stress Induced Hypertension

Received: 19 January 2014     Published: 20 February 2014
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Abstract

Hypertension is an independent risk factor of cardiovascular diseases. Several factors contribute to its development, including chronic stress, which may induce hypertension by increasing sympathetic activity. The signs of increasing sympathetic activity can be primarily detected in the initial phase of hypertension, which is characterized by the increase in cardiac output. In addition to the hemodynamic consequences (increase in cardiac output, tachycardia, coronary vasoconstriction, proarrhythmia), the increase in sympathetic activity has many harmful effects. Numerous metabolic (insulin resistance, dyslipidemia), structural and trophic effects (endothelial dysfunction, vascular hypertrophy, myocardial hypertrophy), as well as thrombotic and humoral processes (procoagulation, enhancement of thrombocyte aggregation, sodium retention, activation of the renin-angiotensin-aldosterone axis) may develop and consequently damage body functions at many targets. Several different antihypertensive drug classes are available for reducing increased sympathetic activity, including peripheral alpha and beta blockers and compounds with central effects. First generation antihypertensive drugs with central mechanisms of action (e.g. clonidine, guanfacine, alpha-methyldopa) is currently rarely administered and only for a few indications as they have a significant adverse events profile. Among second generation compounds with central effects, rilmenidine stimulates imidazoline-1 receptors and thus beneficially influences mild or moderate hypertension that involves enhanced sympathetic nervous system activity.

Published in American Journal of Internal Medicine (Volume 2, Issue 1)
DOI 10.11648/j.ajim.20140201.11
Page(s) 1-5
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2014. Published by Science Publishing Group

Keywords

Sympathetic Nervous System, Stress, Hypertension, Rilmenidine

References
[1] Ezzati M, Lopez AD, Rodgers A, Vander Hoorn S, Murray CJ. Selected major risk factors and global and regional burden of disease. Lancet. 2002;360:1347–1360.
[2] Kearney PM, Whelton M, Reynolds K, Muntner P, Whelton PK, He J. Global burden of hypertension: analysis of worldwide data. Lancet. 2005; 365:217–223.
[3] Wolf-Maier K, Cooper RS, Banegas JR, Giampaoli S, Hense HW, Joffres M, Kastarinen M, Poulter N, Primatesta P, Rodriguez-Artalejo F, Stegmayr B, Thamm M, Tuomilehto J, Vanuzzo D, Vescio F. Hypertension prevalence and blood pressure levels in 6 European countries, Canada, and the United States. JAMA. 2003;289:2363–2369.
[4] Oparil S, Zaman MA, Calhoun DA. Ann Intern Med. 2003;139:761-776
[5] Robert M. Carey, Shetal H. Padia: Physiology and Regulation of the Renin–Angiotensin–Aldosterone System. Textbook of Nephro-Endocrinology, 2009, Pages 147-165
[6] Landsberg L. Diet, obesity and hypertension: an hypothesis involving insulin, the sympathetic nervous system, and adaptive thermogenesis.Q J Med. 1986;61:1081–1090.
[7] Ernsberger P, Damon TH, Graff LM, Schafer SG, Christen MO. Moxonidine, a centrally acting antihypertensive agent, is a selective ligand for I1-imidazoline sites. J Pharmacol Exp Ther. 1993;264:172–182. van Zwieten PA. Central imidazoline (I1) receptors as targets of centrally acting antihypertensives: moxonidine and rilmenidine. J Hypertens. 1997; 15:117–125.
[8] Brook RD, Julius S. Autonomic imbalance, hypertension, and cardiovascular risk. Am J Hypertens 2000;13(6 Pt 2):112S-122S.
[9] Schlaich MP, Kaye DM, Lambert E, Sommerville M, Socratous F, Esler MD. Relation between cardiac sympathetic activity and hypertensive left ventricular hypertrophy. Circulation 2003;108:560–565.
[10] Julius S, Valentini M. Consequences of the increased autonomic nervous drive in hypertensihypertension, heart failure and diabetes. Blood Press 1998;3(Suppl):5–13.
[11] Verrier RL, Antzelevitch C. Autonomic aspects of arrhythogenesis: the enduring and the new. Curr Opin Cardiol 2004;19:2–11.
[12] Curtis BM, O’Keefe JH Jr. Autonomic tone as a cardiovascular risk factor: the dangers of chronic fight or flight.Mayo Clin Proc 2002;77:45–54.
[13] Bousquet P, Feldman J. Drugs acting on imidazoline receptors: a review of their pharmacology, their use in blood pressure control and their potential interest in cardioprotection. Drugs 1999;58:799–812
[14] Roegel JC, Yannoulis N, De Jong W, Monassier L, Feldman J, Bousquet P. Inhibition of centrally induced ventricular arrhythmias by rilmenidine and idazoxan in rabbits. Naunyn Schmiedebergs Arch Pharmacol 1996;354:598–605.
[15] Poisson D, Christen MO, Sannajust F. Protective effects of I(1)- antihypertensive agent moxonidine against neurogenic cardiac arrhythmias in halothane-anesthetized rabbits. J Pharmacol Exp Therap 2000;293:929–938.
[16] Mammoto T, Kamibayashi T, Hayashi Y, Yamatodani A, Takada K, Yoshiya I. Antiarrhythmic action of rilmenidine on adrenaline-induced arrhythmia via central imidazoline receptors in halothane-anaesthetized dogs. Br J Pharmacol 1996;117:1744–1748.
[17] Hayashi Y, Kamibayashi T, Maze M, et al. Role of imidazolinepreferring receptors in the genesis of epinephrine-induced arrhythmias in halothane-anesthetized dogs. Anesthesiology 1993;78:524–530.
[18] Rozanski A, Blumenthal JA, Kaplan J. Impact of psychological factors on the pathogenesis of cardiovascular disease and implications for therapy. Circulation 1999;99:2192–2217.
[19] Panfilov V, Morris AD, Donnelly R, Scemama M, Reid JL. The effects of rilmenidine and atenolol on mental stress, dynamic exercise and autonomic function in mild to moderate hypertension. Br J Clin Pharmacol 1995;40:563–569.
[20] Teixeira de Castro RR, Tibiriçá E, de Oliveira MA, Moreira PB, Catelli MF, Rocha NN, Nóbrega AC. Reduced hemodynamic responses to physical and mental stress under low-dose rilmenidine in healthy subjects. Cardiovasc Drugs Ther. 2006 Apr;20(2):129-34.
[21] Gerin W, Chaplin W, Schwartz JE, Holland J, Alter R, Wheeler R, Duong D, Pickering TG. Sustained blood pressure increase after an acute stressor: the effects of the 11 September 2001 attack on the New York City World Trade Center. J Hypertens. 2005 Feb;23(2):279-84.
[22] Tanja G. M. Vrijkotte; Lorenz J. P. van Doornen; Eco J. C. de Geus. Effects of Work Stress on Ambulatory Blood Pressure, Heart Rate, and Heart Rate Variability. Hypertension. 2000;35:880-886
[23] Opavský J: Autonomní nervový systém a diabetická autonomní neuropatie. Galén, 1. vyd., 2002
[24] Simonyi G, Bedros JR, Medvegy M: Rilmenidine in the Treatment of Hypertensive Obese Patients. Circulation 2010;122;e167 (abstract)
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  • APA Style

    Gábor Simonyi. (2014). Chronic Stress in the Development of Essential Hypertension, Role of Rilmenidine in the Treatment of Stress Induced Hypertension. American Journal of Internal Medicine, 2(1), 1-5. https://doi.org/10.11648/j.ajim.20140201.11

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    ACS Style

    Gábor Simonyi. Chronic Stress in the Development of Essential Hypertension, Role of Rilmenidine in the Treatment of Stress Induced Hypertension. Am. J. Intern. Med. 2014, 2(1), 1-5. doi: 10.11648/j.ajim.20140201.11

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    AMA Style

    Gábor Simonyi. Chronic Stress in the Development of Essential Hypertension, Role of Rilmenidine in the Treatment of Stress Induced Hypertension. Am J Intern Med. 2014;2(1):1-5. doi: 10.11648/j.ajim.20140201.11

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  • @article{10.11648/j.ajim.20140201.11,
      author = {Gábor Simonyi},
      title = {Chronic Stress in the Development of Essential Hypertension, Role of Rilmenidine in the Treatment of Stress Induced Hypertension},
      journal = {American Journal of Internal Medicine},
      volume = {2},
      number = {1},
      pages = {1-5},
      doi = {10.11648/j.ajim.20140201.11},
      url = {https://doi.org/10.11648/j.ajim.20140201.11},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajim.20140201.11},
      abstract = {Hypertension is an independent risk factor of cardiovascular diseases. Several factors contribute to its development, including chronic stress, which may induce hypertension by increasing sympathetic activity. The signs of increasing sympathetic activity can be primarily detected in the initial phase of hypertension, which is characterized by the increase in cardiac output. In addition to the hemodynamic consequences (increase in cardiac output, tachycardia, coronary vasoconstriction, proarrhythmia), the increase in sympathetic activity has many harmful effects. Numerous metabolic (insulin resistance, dyslipidemia), structural and trophic effects (endothelial dysfunction, vascular hypertrophy, myocardial hypertrophy), as well as thrombotic and humoral processes (procoagulation, enhancement of thrombocyte aggregation, sodium retention, activation of the renin-angiotensin-aldosterone axis) may develop and consequently damage body functions at many targets. Several different antihypertensive drug classes are available for reducing increased sympathetic activity, including peripheral alpha and beta blockers and compounds with central effects. First generation antihypertensive drugs with central mechanisms of action (e.g. clonidine, guanfacine, alpha-methyldopa) is currently rarely administered and only for a few indications as they have a significant adverse events profile. Among second generation compounds with central effects, rilmenidine stimulates imidazoline-1 receptors and thus beneficially influences mild or moderate hypertension that involves enhanced sympathetic nervous system activity.},
     year = {2014}
    }
    

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    AU  - Gábor Simonyi
    Y1  - 2014/02/20
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    N1  - https://doi.org/10.11648/j.ajim.20140201.11
    DO  - 10.11648/j.ajim.20140201.11
    T2  - American Journal of Internal Medicine
    JF  - American Journal of Internal Medicine
    JO  - American Journal of Internal Medicine
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    AB  - Hypertension is an independent risk factor of cardiovascular diseases. Several factors contribute to its development, including chronic stress, which may induce hypertension by increasing sympathetic activity. The signs of increasing sympathetic activity can be primarily detected in the initial phase of hypertension, which is characterized by the increase in cardiac output. In addition to the hemodynamic consequences (increase in cardiac output, tachycardia, coronary vasoconstriction, proarrhythmia), the increase in sympathetic activity has many harmful effects. Numerous metabolic (insulin resistance, dyslipidemia), structural and trophic effects (endothelial dysfunction, vascular hypertrophy, myocardial hypertrophy), as well as thrombotic and humoral processes (procoagulation, enhancement of thrombocyte aggregation, sodium retention, activation of the renin-angiotensin-aldosterone axis) may develop and consequently damage body functions at many targets. Several different antihypertensive drug classes are available for reducing increased sympathetic activity, including peripheral alpha and beta blockers and compounds with central effects. First generation antihypertensive drugs with central mechanisms of action (e.g. clonidine, guanfacine, alpha-methyldopa) is currently rarely administered and only for a few indications as they have a significant adverse events profile. Among second generation compounds with central effects, rilmenidine stimulates imidazoline-1 receptors and thus beneficially influences mild or moderate hypertension that involves enhanced sympathetic nervous system activity.
    VL  - 2
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Author Information
  • Metabolic Center, Szent Imre University Teaching Hospital, Budapest, Hungary

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