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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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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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The authors declare no competing financial interests.

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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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