Original Contribution

Am J Hypertens (1996) 9, 113–120; doi: 0895-7061(96)00287-7

Sympathetic Overactivity in Hypertension*

A Moving Target

Stevo Julius1 and Shawna Nesbitt1

1Division of Hypertension, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan, USA

Correspondence: Stevo Julius, MD, ScD, Division of Hypertension, 3918 Taubman Center, University of Michigan Medical Center, Ann Arbor, MI 48109-0356.

*This study was supported in part by a grant from the National Heart, Lung and Blood Institute (HL 37464). The biochemical analyses were performed at the Michigan Diabetes and Training Center, which is the recipient of a grant from the National Institutes of Health (DK 20572).

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Abstract

Considerable progress has been made in our understanding of the role of the nervous system in human hypertension. The evidence for a widespread autonomic abnormality in the early phases of hypertension is overwhelming and excessive sympathetic activity is consistently present in such patients since their childhood. The enhanced sympathetic tone in hypertension is associated with the metabolic syndrome of insulin resistance and dyslipidemia. Multiple mechanisms by which sympathetic overactivity could cause both hypertension and the metabolic syndrome have been documented. Furthermore, the excessive sympathetic tone is conducive to coronary heart disease through its association with high hematocrit values and with excessive platelet aggregability.

Surprisingly, the myth that patients with neurogenic hypertension have a benign prognosis continues to persist. Much of the misunderstanding stems from the idea that patients with neurogenic hypertension, commonly called "white coat" or borderline hypertension, do not develop established hypertension. There is no support for such an assessment; in fact, patients with neurogenic hypertension are at a high risk of future accelerated hypertension. Another misunderstanding relates to differences in hemodynamics between neurogenic and established hypertension. It is true that patients with neurogenic hypertension initially show an increase of cardiac output. However, this later evolves into a classic picture of established high resistance hypertension. The hemodynamic transition is secondary to a decrease in cardiac responsiveness and an increase in vascular responsiveness over the course of hypertension.

With passage of time, vascular reactivity increases, yet sympathetic tone tends to decrease. This can be explained by the "blood pressure seeking behavior of the central nervous system." In hypertension, the central nervous system appears to seek a higher blood pressure level and, as the vasculature becomes hyperresponsive, less sympathetic tone is needed to maintain the elevated blood pressure. This decrease of sympathetic tone in later phases of hypertension should not be viewed as a normalization, since sympathetic tone in relationship to vascular hyperresponsiveness remains excessive and the central nervous system maintains a crucial role in sustaining high blood pressure in hypertension. Am J Hypertens 1996;9:113S-120S

Keywords:

White coat hypertension, sympathetic nervous system, blood pressure

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