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Vol 20, No 1 (2016)
Review paper
Published online: 2016-03-31
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Role of autonomic nervous system in the pathomechanism of hypertension

Michał Zamojski, Zbigniew Dubielski, Bartosz Wiechecki, Olga Możeńska, Jan Gieraltowski, Dariusz Artur Kosior
DOI: 10.5603/AH.2016.0005
·
Arterial Hypertension 2016;20(1):21-25.

open access

Vol 20, No 1 (2016)
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Published online: 2016-03-31

Abstract

Due to high prevalence of hypertension (HT) in worldwide population, all aspects of this disease are studied in order to understand its pathogenesis and the influence on human body, as well as in order to find proper treatment. Impaired balance of autonomic nervous system (ANS) is taken into account as one of the main causes elevating blood pressure (BP). It seems that over-activation of sympathetic nervous system (SNS) is the most important factor in pathogenesis of HT. There are some methods which allow us to measure the sympathetic and parasympathetic nervous system activity. Some of them are described below and the influence of impaired ANS balance on HT development is presented. Many different, natural and pathologic factors can cause SNS response, so the measurement of the sole ANS activity cannot fully answer the question about the pathomechanism underlying HT. In this paper, we present some hypotheses regarding possible mechanisms of the disease progression. In primary HT, impairment of baroreceptors response is considered one of such mechanisms. Another one is the influence of hyperinsulinemia on the activation of SNS in insulin resistant patients. A few other factors are considered, like obesity, salt intake, sodium retention and alcohol intake and they are described briefly in our paper. In secondary hypertension, SNS can be activated indirectly by comorbidities, and this pathomechanism is also discussed.

Abstract

Due to high prevalence of hypertension (HT) in worldwide population, all aspects of this disease are studied in order to understand its pathogenesis and the influence on human body, as well as in order to find proper treatment. Impaired balance of autonomic nervous system (ANS) is taken into account as one of the main causes elevating blood pressure (BP). It seems that over-activation of sympathetic nervous system (SNS) is the most important factor in pathogenesis of HT. There are some methods which allow us to measure the sympathetic and parasympathetic nervous system activity. Some of them are described below and the influence of impaired ANS balance on HT development is presented. Many different, natural and pathologic factors can cause SNS response, so the measurement of the sole ANS activity cannot fully answer the question about the pathomechanism underlying HT. In this paper, we present some hypotheses regarding possible mechanisms of the disease progression. In primary HT, impairment of baroreceptors response is considered one of such mechanisms. Another one is the influence of hyperinsulinemia on the activation of SNS in insulin resistant patients. A few other factors are considered, like obesity, salt intake, sodium retention and alcohol intake and they are described briefly in our paper. In secondary hypertension, SNS can be activated indirectly by comorbidities, and this pathomechanism is also discussed.

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Keywords

sympathetic nervous system; parasympathetic nervous system; essential hypertension; sympathetic activation; catecholamines

About this article
Title

Role of autonomic nervous system in the pathomechanism of hypertension

Journal

Arterial Hypertension

Issue

Vol 20, No 1 (2016)

Article type

Review paper

Pages

21-25

Published online

2016-03-31

Page views

1129

Article views/downloads

2120

DOI

10.5603/AH.2016.0005

Bibliographic record

Arterial Hypertension 2016;20(1):21-25.

Keywords

sympathetic nervous system
parasympathetic nervous system
essential hypertension
sympathetic activation
catecholamines

Authors

Michał Zamojski
Zbigniew Dubielski
Bartosz Wiechecki
Olga Możeńska
Jan Gieraltowski
Dariusz Artur Kosior

References (54)
  1. Mancia G, Fagard R, Narkiewicz K, et al. 2013 ESH/ESC Guidelines for the management of arterial hypertension. Journal of Hypertension. 2013; 31(7): 1281–1357.
    CrossRef
  2. Messerli FH, Williams B, Ritz E. Essential hypertension. Lancet. 2007; 370(9587): 591–603.
    CrossRefPubMed
  3. Carretero OA, Oparil S. Essential hypertension. Part I: definition and etiology. Circulation. 2000; 101(3): 329–335.
    PubMed
  4. Raj M, Krishnakumar R. Hypertension in children and adolescents: epidemiology and pathogenesis. Indian J Pediatr. 2013; 80 Suppl 1: S71–S76.
    CrossRefPubMed
  5. Ehret GB, Munroe PB, Rice KM, et al. International Consortium for Blood Pressure Genome-Wide Association Studies, CARDIoGRAM consortium, CKDGen Consortium, KidneyGen Consortium, EchoGen consortium, CHARGE-HF consortium. Genetic variants in novel pathways influence blood pressure and cardiovascular disease risk. Nature. 2011; 478(7367): 103–109.
    CrossRefPubMed
  6. Grassi G, Seravalle G, Trevano FQ, et al. Neurogenic abnormalities in masked hypertension. Hypertension. 2007; 50(3): 537–542.
    CrossRefPubMed
  7. Grassi G, Seravalle G, Dell'Oro R, et al. Adrenergic and reflex abnormalities in obesity-related hypertension. Hypertension. 2000; 36(4): 538–542.
    PubMed
  8. Pullalarevu R, Akbar G, Teehan G. Secondary hypertension, issues in diagnosis and treatment. Prim Care. 2014; 41(4): 749–764.
    CrossRefPubMed
  9. Julius S, Pascual AV, London R. Role of parasympathetic inhibition in the hyperkinetic type of borderline hypertension. Circulation. 1971; 44(3): 413–418.
    PubMed
  10. Grassi G, Cattaneo BM, Seravalle G, et al. Baroreflex impairment by low sodium diet in mild or moderate essential hypertension. Hypertension. 1997; 29(3): 802–807.
    PubMed
  11. Esler M, Jennings G, Lambert G. Noradrenaline release and the pathophysiology of primary human hypertension. Am J Hypertens. 1989; 2(3 Pt 2): 140S–146S.
    PubMed
  12. Solt VB, Brown MR, Kennedy B, et al. Elevated insulin, norepinephrine, and neuropeptide Y in hypertension. Am J Hypertens. 1990; 3(11): 823–828.
    PubMed
  13. Jones P, Dauger S, Peters MJ. Bradycardia during critical care intubation: mechanisms, significance and atropine. Arch Dis Child. 2012; 97(2): 139–144.
    CrossRefPubMed
  14. Goldstein DS. Plasma catecholamines and essential hypertension. An analytical review. Hypertension. 1983; 5(1): 86–99.
    CrossRef
  15. Kratz A, Ferraro M, Sluss PM, et al. Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Laboratory reference values. N Engl J Med. 2004; 351(15): 1548–1563.
    CrossRefPubMed
  16. Esler M, Lambert G, Jennings G, et al. Regional norepinephrine turnover in human hypertension. Clin Exp Hypertens A. 1989; 11 Suppl 1(3 Pt 2): 75–89.
    PubMed
  17. Mancia G, Grassi G, Ferrari AU. Reflex control of the circulation in experimental and human hypertension. In: Zanchetti A, Mancia G. ed. Handbook of Hypertension, Vol 17: Pathophysiology of Hypertension. Elsevier Science, Amsterdam 1997: 568–601.
  18. Grassi G. Adrenergic overdrive as the link among hypertension, obesity, and impaired thermogenesis: lights and shadows. Hypertension. 2007; 49(1): 5–6.
    CrossRefPubMed
  19. Fukiyama K, McCubbin JW, Page IH. Chronic hypertension elicited by infusion of angiotensin into vertebral arteries of unanaesthetized dogs. Clin Sci. 1971; 40(3): 283–291.
    PubMed
  20. Ha SK. Dietary salt intake and hypertension. Electrolyte Blood Press. 2014; 12(1): 7–18.
    CrossRefPubMed
  21. Bock A. [The influence of salt intake on hypertension]. Ther Umsch. 2009; 66(11): 721–724.
    CrossRefPubMed
  22. Lurbe E, Redon J, Kesani A, et al. Increase in nocturnal blood pressure and progression to microalbuminuria in type 1 diabetes. N Engl J Med. 2002; 347(11): 797–805.
    CrossRefPubMed
  23. Dustan HP, Valdes G, Bravo EL, et al. Excessive sodium retention as a characteristic of salt-sensitive hypertension. Am J Med Sci. 1986; 292(2): 67–74.
    PubMed
  24. Howes LG, Reid JL. The effects of alcohol on local, neural and humoral cardiovascular regulation. Clin Sci (Lond). 1986; 71(1): 9–15.
    PubMed
  25. Rupp H, Brilla CG, Maisch B. [Hypertension and alcohol: central and peripheral mechanisms]. Herz. 1996; 21(4): 258–264.
    PubMed
  26. Grassi G. Role of the sympathetic nervous system in human hypertension. J Hypertens. 1998; 16(Supplement): 1979–1987.
    CrossRef
  27. Scherrer U, Sartori C. Insulin as a vascular and sympathoexcitatory hormone: implications for blood pressure regulation, insulin sensitivity, and cardiovascular morbidity. Circulation. 1997; 96(11): 4104–4113.
    PubMed
  28. Anderson EA, Balon TW, Hoffman RP, et al. Insulin increases sympathetic activity but not blood pressure in borderline hypertensive humans. Hypertension. 1992; 19(6_Pt_2): 621–627.
    CrossRef
  29. Hossain P, Kawar B, El Nahas M. Obesity and diabetes in the developing world--a growing challenge. N Engl J Med. 2007; 356(3): 213–215.
    CrossRefPubMed
  30. Rocchini AP, Yang JQ, Gokee A. Hypertension and insulin resistance are not directly related in obese dogs. Hypertension. 2004; 43(5): 1011–1016.
    CrossRefPubMed
  31. Wofford MR, Hall JE. Pathophysiology and treatment of obesity hypertension. Curr Pharm Des. 2004; 10(29): 3621–3637.
    PubMed
  32. Hou R, Liu Z, Liu J, et al. The circadian rhythm of blood pressure and the effect of salt intake in salt-sensitive subjects. Chin Med J (Engl). 2000; 113(1): 22–26.
    PubMed
  33. Sullivan JM. Salt sensitivity. Definition, conception, methodology, and long-term issues. Hypertension. 1991; 17(1 Suppl): I61–I68.
    PubMed
  34. Campese VM, Romoff MS, Levitan D, et al. Abnormal relationship between sodium intake and sympathetic nervous system activity in salt-sensitive patients with essential hypertension. Kidney Int. 1982; 21(2): 371–378.
    PubMed
  35. Spallone V, Gambardella S, Maiello MR, et al. Relationship between autonomic neuropathy, 24-h blood pressure profile, and nephropathy in normotensive IDDM patients. Diabetes Care. 1994; 17(6): 578–584.
    PubMed
  36. Ripoli A, Pingitore A, Favilli B, et al. Does subclinical hypothyroidism affect cardiac pump performance? Evidence from a magnetic resonance imaging study. J Am Coll Cardiol. 2005; 45(3): 439–445.
    CrossRefPubMed
  37. Richelsen B, Sørensen NS. Alpha 2- and beta-adrenergic receptor binding and action in gluteal adipocytes from patients with hypothyroidism and hyperthyroidism. Metabolism. 1987; 36(11): 1031–1039.
    PubMed
  38. Mancia G, Sega R, Bravi C, et al. Ambulatory blood pressure normality. J Hypertens. 1995; 13(12): 1377–1390.
    CrossRef
  39. Pedrosa RP, Drager LF, Gonzaga CC, et al. Obstructive sleep apnea: the most common secondary cause of hypertension associated with resistant hypertension. Hypertension. 2011; 58(5): 811–817.
    CrossRefPubMed
  40. Williams RS, Lefkowitz RJ. The effect of thyroid hormone on adrenergic receptors. In: Oppenheimer JH. ed. Molecular Basis of Thyroid Hormone Action. Academic Press, London 1983: 325–349.
  41. Gennari C, Nami R, Gonnelli S. Hypertension and primary hyperparathyroidism: the role of adrenergic and renin-angiotensin-aldosterone systems. Miner Electrolyte Metab. 1995; 21(1-3): 77–81.
    PubMed
  42. Welch WJ. The pathophysiology of renin release in renovascular hypertension. Semin Nephrol. 2000; 20(5): 394–401.
    PubMed
  43. Ram CV, Clagett GP, Radford LR. Renovascular hypertension. Semin Nephrol. 1995; 15: 152–174.
  44. Somers VK, Dyken ME, Clary MP, et al. Sympathetic neural mechanisms in obstructive sleep apnea. J Clin Invest. 1995; 96(4): 1897–1904.
    CrossRefPubMed
  45. Seif F, Patel SR, Walia HK, et al. Obstructive sleep apnea and diurnal nondipping hemodynamic indices in patients at increased cardiovascular risk. J Hypertens. 2014; 32(2): 267–275.
    CrossRefPubMed
  46. Kario K, Schwartz JE, Gerin W, et al. Ambulatory physical activity as a determinant of diurnal blood pressure variation. Hypertension. 1999; 34(4 Pt 1): 685–691.
    PubMed
  47. Fava C, Montagnana M, Favaloro EJ, et al. Obstructive sleep apnea syndrome and cardiovascular diseases. Semin Thromb Hemost. 2011; 37(3): 280–297.
    CrossRefPubMed
  48. Fletcher EC, Miller J, Schaaf JW, et al. Urinary catecholamines before and after tracheostomy in patients with obstructive sleep apnea and hypertension. Sleep. 1987; 10(1): 35–44.
    PubMed
  49. Parati G, Di Rienzo M, Bonsignore MR, et al. Autonomic cardiac regulation in obstructive sleep apnea syndrome: evidence from spontaneous baroreflex analysis during sleep. J Hypertens. 1997; 15(12 Pt 2): 1621–1626.
    PubMed
  50. Swislocki AL, Hoffman BB, Reaven GM. Insulin resistance, glucose intolerance and hyperinsulinemia in patients with hypertension. Am J Hypertens. 1989; 2(6 Pt 1): 419–423.
    PubMed
  51. Narkiewicz K, Pesek CA, Kato M, et al. Baroreflex control of sympathetic nerve activity and heart rate in obstructive sleep apnea. Hypertension. 1998; 32(6): 1039–1043.
    PubMed
  52. Chen J, He L, Dinger B, et al. Cellular mechanisms involved in rabbit carotid body excitation elicited by endothelin peptides. Respir Physiol. 2000; 121(1): 13–23.
    PubMed
  53. Chen J, He L, Dinger B, et al. Role of endothelin and endothelin A-type receptor in adaptation of the carotid body to chronic hypoxia. Am J Physiol Lung Cell Mol Physiol. 2002; 282(6): L1314–L1323.
    CrossRefPubMed
  54. Gong M, Hubner N. Molecular genetics of human hypertension. Clin Sci (Lond). 2006; 110(3): 315–326.
    CrossRefPubMed

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