Skip to main content
Log in

Obstructive sleep apnea as a cause of neurogenic hypertension

  • Published:
Current Hypertension Reports Aims and scope Submit manuscript

Abstract

Abnormalities in neural circulatory control may contribute importantly to the hypertensive state. The sympathetic nervous system in particular is a key mechanism for increasing blood pressure. Patients with obstructive sleep apnea have increased sympathetic activity. Obesity or other coexisting disease states do not explain the heightened sympathetic drive. This review examines the evidence linking sleep apnea with hypertension and the possible role of excessive sympathetic drive as a mediator of higher blood pressure in sleep apnea. Abnormalities in reflex circulatory control that could act to increase sympathetic activity in sleep apnea are also discussed.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Similar content being viewed by others

References and Recommended Reading

  1. DiBonaGF: Sympathetic neural control of the kidney in hypertension. Hypertension 1990, 19:I28-I35.

    Google Scholar 

  2. Abel PW, Hermsmeyer K: Sympathetic cross-innervation of SHR and genetic controls suggests a trophic influence on vascular muscle membranes. Circ Res 1981, 49:1311–1318.

    PubMed  CAS  Google Scholar 

  3. Chapleau MW, Abboud FM: Mechanism of adaptation and resetting of the baroreceptor reflex. In Cardiovascular Reflex Control in Health and Disease Edited by R Hainsworth and AL Mark. London: WB Saunders;1993:165–193.

    Google Scholar 

  4. Goldstein DS: Plasma catecholamine and essential hypertension: an analytical review. Hypertension 1983, 5:86–99. This is an extensive review of studies looking at the relationship between catecholamine levels and BP levels. A synthesis of the evidence available at the time was suggestive of higher catecholamine levels in essential hypertension.

    PubMed  CAS  Google Scholar 

  5. Esler M, Jennings G, Lambert G: Noradrenaline release and the pathophysiology of primary human hypertension. Am J Hypertens 1989, 2:140S-146S.

    PubMed  CAS  Google Scholar 

  6. Somers VK, Mark AL, Abboud FM: Potentiation of sympathetic nerve responses to hypoxia in borderline hypertensive subjects. Hypertension 1988, 11:608–612. In a controlled study of the effects of hypoxia on sympathetic drive, patients with borderline hypertension had about twofold greater sympathetic activation during hypoxia than in control subjects. During apnea and hypoxia, the potentiated response in hypertension was especially evident, with sympathetic neural activity in hypertensive subjects averaging about twelve times the response seen in control subjects.

    PubMed  CAS  Google Scholar 

  7. Rea RF, Hamdan M: Baroreflex control of muscle sympathetic nerve activity in borderline hypertension. Circulation 1990, 82:856–862.

    PubMed  CAS  Google Scholar 

  8. Anderson EA, Sinkey CA, Lawton WJ, Mark AL: Elevated sympathetic nerve activity in borderline hypertensive humans: evidence from direct intraneural recordings. Hypertension 1989, 14:177–183.

    PubMed  CAS  Google Scholar 

  9. Matsukawa T, Mano T, Gotoh E, Ishii M: Elevated sympathetic nerve activity in patients with accelerated essential hypertension. J Clin Invest 1993, 92:25–28.

    PubMed  CAS  Google Scholar 

  10. Miyajima E, Yamada Y, Yoshida Y, et al.: Muscle sympathetic nerve activity in renovascular hypertension and primary aldosteronism. Hypertension 1991, 17:1057–1062.

    PubMed  CAS  Google Scholar 

  11. Converse RL, Jacobsen TN, Toto RD, et al.: Sympathetic overactivity in patients with chronic renal failure. New Engl J Med 1992, 327:1912–1918.

    Article  PubMed  Google Scholar 

  12. Scherrer U, Vissing SF, Morgan BJ, et al.: Cyclosporine-induced sympathetic activation and hypertension after heart transplantation. New Engl J Med 1990, 323:693–699. This study tested the hypothesis that cyclosporine increased sympathetic drive, thus contributing to the increased BP levels that are so frequently evident in patients after heart transplantation.

    Article  PubMed  CAS  Google Scholar 

  13. Schobel HP, Fischer T, Heuszer K, et al.: Preeclampsia-a state of sympathetic overactivity. New Engl J Med 1996, 335:1480–1485. This study of sympathetic activity in normal and preeclamptic pregnant females provided further evidence for the involvement of the sympathetic nervous system in secondary hypertension. Sympathetic activity was higher in the preeclamptic females and declined after delivery, together with the expected decrease in BP levels.

    Article  PubMed  CAS  Google Scholar 

  14. Kales A, Cadieux RJ, Shaw LC, et al.: Sleep apnea in a hypertensive population. Lancet 1984, 2:1005–1008.

    Article  PubMed  CAS  Google Scholar 

  15. Koskenvuo M, Kaprio J, Partinen M, et al.: Snoring as a risk factor for hypertension and angina pectoris. Lancet 1985, 1:89–95.

    Google Scholar 

  16. Brooks D, Horner RL, Kozar LF, et al.: Obstructive sleep apnea as a cause of systemic hypertension: evidence from a canine model. J Clin Invest 1997, 99:106–109. Simulated obstructive sleep apnea in a canine model resulted in significant increases inBP levels. The sustained BP increase was likely secondary to repetitive episodes of hypoxemia during obstructive sleep apnea.

    PubMed  CAS  Google Scholar 

  17. Young T, Finn L, Hla KM, et al.: Snoring as a part of a doseresponse relationship between sleep-disordered breathing and blood pressure. Sleep 1996, 19:S202-S205.

    PubMed  CAS  Google Scholar 

  18. Somers VK, Zavala DC, Mark AL, Abboud FM: Influence of ventilation and hypocapnia on sympathetic nerve responses to hypoxia in normal humans. J Appl Physiol 1989, 67:2095–2100. This study showed that decreases in blood oxygen levels induced increases in sympathetic activity, and that the increased ventilation inhibited the sympathetic response to hypoxia. Apnea during hypoxia markedly increased sympathetic activity.

    PubMed  CAS  Google Scholar 

  19. Somers VK, Zavala DC, Mark AL, Abboud FM:Contrasting effects of hypoxia and hypercapnia on ventilation and sympathetic activity in humans. J Appl Physiol 1989, 67:2101–2106.

    PubMed  CAS  Google Scholar 

  20. Przybylski J, Trzebski A, Czyzewski T, Jodkowski J: Responses to hyperoxia, hypoxia, hypercapnia and almitrine in spontaneously hypertensive rats. Bull Eur Physiopathol Respir 1982, 18:145–154.

    CAS  Google Scholar 

  21. Trzebski A, Tafil M, Zoltowski M, Przybylski J: Increased sensitivity of the arterial chemoreceptor drive in young men with mild hypertension. Cardiovasc Res 1982, 16:163–172.

    Article  PubMed  CAS  Google Scholar 

  22. Fletcher EC, Miller J, Schaaf JW, Fletcher JG: Urinary catecholamines before and after tracheostomy in patients with obstructive sleep apnea and hypertension. Sleep 1987, 10:35–44.

    PubMed  CAS  Google Scholar 

  23. Marrone O, Riccobono L, Salvaggio A, et al.: Catecholamines and blood pressure in obstructive sleep apnea syndrome. Chest 1993, 103:722–727.

    PubMed  CAS  Google Scholar 

  24. Hedner J, Ejnell H, Sellgren J, et al.: Is high and fluctuating muscle nerve sympathetic activity in the sleep apnoea syndrome of pathogenetic importance for the development of hypertension? J Hypertens 1988, 6(suppl):529-S531.

    Google Scholar 

  25. Somers VK, Dyken ME, Clary MP, Abboud FM: Sympathetic neural mechanisms in obstructive sleep apnea. J Clin Invest 1995, 96:1897–1904. Patients with sleep apnea had high levels of sympathetic activity even during normoxic wakefulness. During obstructive apnea during sleep, both sympathetic activity and BP levels increased further. Treatment of sleep apnea with CPAP markedly reduced BP levels and sympathetic activity during sleep.

    PubMed  CAS  Google Scholar 

  26. Palatini P, Julius S: Heart rate and cardiovascular risk. J Hypertens 1997, 15:3–17. This review examines the relationship between heart rate and cardiovascular events and proposes heart rate as an important independent risk factor for cardiovascular disease.

    Article  PubMed  CAS  Google Scholar 

  27. Singh JP, Larson MG, Tsuji H, et al.: Reduced heart rate variability: a risk factor for new onset hypertension [abstract]. Circulation 1997, 96:I406.

    Google Scholar 

  28. Narkiewicz K, Montano N, Cogliati C, et al.: Altered cardiovascular variability in obstructive sleep apnea. Circulation 1998, 98:1071–1077.

    PubMed  CAS  Google Scholar 

  29. Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology: Heart rate variability: standards of measurement, physiological interpretation, and clinical use. Circulation 1996, 93:1043–1065.

    Google Scholar 

  30. Frattola A, Parati G, Cuspidi C, et al.: Prognostic value of 24-hour blood pressure variability. J Hypertens 1993, 11:1133–1137.

    Article  PubMed  CAS  Google Scholar 

  31. Palatini P, Penzo M, Racioppa A, et al.: Clinical relevance of nighttime blood pressure and of daytime blood pressure variability. Arch Int Med 1992, 152:1855–1860.

    Article  CAS  Google Scholar 

  32. Van Vliet BN, Hu L, Scott T, et al.: Cardiac hypertrophy and telemetered blood pressure 6 wk after baroreceptor denervation in normotensive rats. Am J Physiol 1996, 271:R1759–1769.

    PubMed  CAS  Google Scholar 

  33. Narkiewicz K, van de Borne PJH, Montano N, et al.: Contribution of tonic chemoreflex activation to sympathetic activity and blood pressure in patients with obstructive sleep apnea. Circulation 1998, 97:943–945.

    PubMed  CAS  Google Scholar 

  34. Hornyak MM, Cejnar M, Elam M, et al.: Sympathetic muscle nerve activity during sleep in man. Brain 1991, 114:1281–1295.

    Article  PubMed  Google Scholar 

  35. Okada H, Iwase S, Mano T, et al.: Changes in muscle sympathetic nerve activity in sleep during sleep in humans. Neurology 1991, 41:1961–1966.

    PubMed  CAS  Google Scholar 

  36. Somers VK, Dyken ME, Mark AL, Abboud FM: Sympathetic nerve activity during sleep in normal humans. N Engl J Med 1993, 328:303–307. Sympathetic activity decreased during non-REM sleep together with BP levels and heart rate. The decrease was enhanced with progressively deepening sleep stages from Stage I through to Stage IV. During REM sleep there was a marked increase in sympathetic nerve traffic with intermittent surges in BP and heart rate.

    Article  PubMed  CAS  Google Scholar 

  37. Suzuki M, Otsuka K, Guilleminault C: Long-term nasal continuous positive airway pressure administration can normalize hypertension in obstructive sleep apnea patients. Sleep 1993, 16:545–549.

    PubMed  CAS  Google Scholar 

  38. Wilcox I, Grunstein RR, Hedner JA, et al.: Effect of nasal continuous positive airway pressure during sleep on 24-hour blood pressure in obstructive sleep apnea. Sleep 1993, 16:539–544.

    PubMed  CAS  Google Scholar 

  39. Waradekar NV, Sinoway LI, Zwillich CW, Leuenberger UA: Influence of treatment on muscle sympathetic nerve activity in sleep apnea. Am J Respir Crit Care Med 1996, 153:1333–1338.

    PubMed  CAS  Google Scholar 

  40. Phillips BG, Narkiewicz K, Pesek CA, et al.: Effects of obstructive sleep apnea on endothelin-1 and blood pressure. J Hypertens 1999, 17:61–66.

    PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Rights and permissions

Reprints and permissions

About this article

Cite this article

Narkiewicz, K., Somers, V.K. Obstructive sleep apnea as a cause of neurogenic hypertension. Current Science Inc 1, 268–273 (1999). https://doi.org/10.1007/s11906-999-0032-7

Download citation

  • Issue Date:

  • DOI: https://doi.org/10.1007/s11906-999-0032-7

Keywords

Navigation