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Orthostatic hypertension: when pressor reflexes overcompensate

Abstract

Orthostatic hypertension—a rise in blood pressure upon assuming upright posture—is an underappreciated and understudied clinical phenomenon. There is currently no widely agreed-upon definition of clinical orthostatic hypertension, the current definitions being operational within the context of particular studies. The underlying pathophysiology is thought to involve activation of the sympathetic nervous system, but the actual etiology is poorly understood. Orthostatic hypertension is observed in association with a variety of other clinical conditions, including essential hypertension, dysautonomias, and type 2 diabetes mellitus. Orthostatic hypertension has been associated with increased occurrence of silent cerebrovascular ischemia and possibly with neuropathy in type 2 diabetes. So, appreciation of the true incidence of orthostatic hypertension, elucidation of the underlying pathophysiology, and an understanding of potentially effective treatment approaches and their associated risks and benefits might all have major clinical significance. Orthostatic hypertension is an aspect of hypertension that is in need of further focused investigation.

Key Points

  • Orthostatic hypertension—in contrast to orthostatic hypotension—is an understudied and often overlooked form of blood pressure dysregulation

  • There is no generally accepted definition of orthostatic hypertension; an increase in systolic blood pressure of 20 mmHg or more upon standing has been proposed

  • Physiological processes that might underlie orthostatic hypertension include excessive venous pooling leading to decreased cardiac output, activation of the sympathetic nervous system, and increased levels of circulating hormones

  • Orthostatic hypertension is a feature of several conditions and patient subgroups, including essential hypertension in the elderly and 'extreme dippers', dysautonomias, and pheochromocytoma

  • In the absence of data on specific therapies, management of orthostatic hypertension should be a function mainly of the condition of which it is a feature, and might include adrenergic receptor antagonists

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Figure 1: Pathophysiological mechanisms proposed to underlie orthostatic hypertension.

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References

  1. Izzo JL Jr and Taylor AA (1999) The sympathetic nervous system and baroreflexes in hypertension and hypotension. Curr Hypertens Rep 1: 254–263

    Article  Google Scholar 

  2. Jacob G et al. (1998) Effect of standing on neurohumoral responses and plasma volume in healthy subjects. J Appl Physiol 84: 914–921

    Article  CAS  Google Scholar 

  3. Robertson D et al. (1998) Distribution and observed associations of orthostatic blood pressure changes in elderly general medicine outpatients. Am J Med Sci 315: 287–295

    Article  CAS  Google Scholar 

  4. Jacob G and Robertson D (1995) Orthostatic hypotension: epidemiology, pathophysiology and management. Curr Opin Nephrol Hypertens 4: 452–454

    Article  CAS  Google Scholar 

  5. Robertson D and Davis TL (1995) Recent advances in the treatment of orthostatic hypotension. Neurology 45: S26–32

    Article  CAS  Google Scholar 

  6. Goldstein DS et al. (2003) Association between supine hypertension and orthostatic hypotension in autonomic failure. Hypertension 42: 136–142

    Article  CAS  Google Scholar 

  7. Johnson RH (1983) Autonomic dysfunction in clinical disorders with particular reference to catecholamine release. J Auton Nerv Syst 7: 219–232

    Article  CAS  Google Scholar 

  8. Carruthers SG (1994) Adverse effects of alpha 1-adrenergic blocking drugs. Drug Saf 11: 12–20

    Article  CAS  Google Scholar 

  9. Pearce CJ and Wallin JD (1994) Labetalol and other agents that block both alpha- and beta-adrenergic receptors. Cleve Clin J Med 61: 59–69

    Article  CAS  Google Scholar 

  10. Heusser K et al. (2005) Baroreflex failure. Hypertension 45: 834–839

    Article  CAS  Google Scholar 

  11. Robertson D et al. (1993) The diagnosis and treatment of baroreflex failure. N Engl J Med 329: 1449–1455

    Article  CAS  Google Scholar 

  12. Ketch T et al. (2002) Four faces of baroreflex failure: hypertensive crisis, volatile hypertension, orthostatic tachycardia, and malignant vagotonia. Circulation 105: 2518–2523

    Article  Google Scholar 

  13. Manger WM (1993) Baroreflex failure—a diagnostic challenge. N Engl J Med 329: 1494–1495

    Article  CAS  Google Scholar 

  14. Jordan J et al. (1998) Raised cerebrovascular resistance in idiopathic orthostatic intolerance: evidence for sympathetic vasoconstriction. Hypertension 32: 699–704

    Article  CAS  Google Scholar 

  15. Jacob G et al. (1999) Effects of standing on cerebrovascular resistance in patients with idiopathic orthostatic intolerance. Am J Med 106: 59–64

    Article  CAS  Google Scholar 

  16. Robertson RM et al. (1980) Ergonovine-induced discrepancy between direct and indirect arterial-pressure recording. Clin Res 28: A242

    Google Scholar 

  17. Nicholson JP Jr et al. (1983) Pheochromocytoma and prazosin. Ann Intern Med 99: 477–479

    Article  Google Scholar 

  18. Ram CV and Engelman K (1979) Pheochromocytoma—recognition and management. Curr Probl Cardiol 4: 1–37

    Article  CAS  Google Scholar 

  19. Shibao C et al. (2005) Hyperadrenergic postural tachycardia syndrome in mast cell activation disorders. Hypertension 45: 385–390

    Article  CAS  Google Scholar 

  20. Eguchi K et al. (2004) Greater change of orthostatic blood pressure is related to silent cerebral infarct and cardiac overload in hypertensive subjects. Hypertens Res 27: 235–241

    Article  Google Scholar 

  21. Kario K et al. (2002) U-curve relationship between orthostatic blood pressure change and silent cerebrovascular disease in elderly hypertensives: orthostatic hypertension as a new cardiovascular risk factor. J Am Coll Cardiol 40: 133–141

    Article  Google Scholar 

  22. Streeten DH et al. (1985) Orthostatic hypertension: pathogenetic studies. Hypertension 7: 196–203

    Article  CAS  Google Scholar 

  23. Kario K et al. (1998) Relationship between extreme dippers and orthostatic hypertension in elderly hypertensive patients. Hypertension 31: 77–82

    Article  CAS  Google Scholar 

  24. Kario K and Shimada K (2004) Risers and extreme-dippers of nocturnal blood pressure in hypertension: antihypertensive strategy for nocturnal blood pressure. Clin Exp Hypertens 26: 177–189

    Article  Google Scholar 

  25. Matsubayashi K et al. (1997) Postural dysregulation in systolic blood pressure is associated with worsened scoring on neurobehavioral function tests and leukoaraiosis in the older elderly living in a community. Stroke 28: 2169–2173

    Article  CAS  Google Scholar 

  26. Jordan J et al. (1997) Malignant vagotonia due to selective baroreflex failure. Hypertension 30: 1072–1077

    Article  CAS  Google Scholar 

  27. Jordan J et al. (2000) Severely impaired baroreflex-buffering in patients with monogenic hypertension and neurovascular contact. Circulation 102: 2611–2618

    Article  CAS  Google Scholar 

  28. Smit AA et al. (2002) Long-term effects of carotid sinus denervation on arterial blood pressure in humans. Circulation 105: 1329–1335

    Article  Google Scholar 

  29. Timmers HJ et al. (2004) Cardiovascular responses to stress after carotid baroreceptor denervation in humans. Ann N Y Acad Sci 1018: 515–519

    Article  Google Scholar 

  30. Shannon JR et al. (2000) Orthostatic intolerance and tachycardia associated with norepinephrine-transporter deficiency. N Engl J Med 342: 541–549

    Article  CAS  Google Scholar 

  31. Yoshinari M et al. (2001) Orthostatic hypertension in patients with type 2 diabetes. Diabetes Care 24: 1783–1786

    Article  CAS  Google Scholar 

  32. Jannetta PJ et al. (1985) Neurogenic hypertension: etiology and surgical treatment. I: observations in 53 patients. Ann Surg 201: 391–398

    Article  CAS  Google Scholar 

  33. Levy EI et al. (1998) Microvascular decompression of the left lateral medulla oblongata for severe refractory neurogenic hypertension. Neurosurgery 43: 1–6

    Article  CAS  Google Scholar 

  34. Streeten DH et al. (1988) Abnormal orthostatic changes in blood pressure and heart rate in subjects with intact sympathetic nervous function: evidence for excessive venous pooling. J Lab Clin Med 111: 326–335

    CAS  PubMed  Google Scholar 

  35. Jacob G et al. (2000) The neuropathic postural tachycardia syndrome. N Engl J Med 343: 1008–1014

    Article  CAS  Google Scholar 

  36. Raffai G et al. (2005) Experimental orthostasis elicits sustained hypertension, which can be prevented by sympathetic blockade in the rat. J Cardiovasc Pharmacol 45: 354–361

    Article  CAS  Google Scholar 

Download references

Acknowledgements

The authors are supported by PHS Grants NIH MO1 RR00095, 5P01 HL56693 and R01 HL71784.

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Correspondence to David Robertson.

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Fessel, J., Robertson, D. Orthostatic hypertension: when pressor reflexes overcompensate. Nat Rev Nephrol 2, 424–431 (2006). https://doi.org/10.1038/ncpneph0228

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