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Cited by 237Blood Pressure and Hypertension StudiesHeart Rate Variability and Autonomic ControlCardiovascular Syncope and Autonomic Disorders

Sympathetic overactivity in hypertension. A moving target

JULIUS, S, NESBITT, S·1996·American Journal of Hypertension
DOI 10.1016/0895-7061(96)00287-7
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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.

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Crossref · 10.1016/0895-7061(96)00287-7

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  • In essential hypertension, elevated arterial pressure has been associated with increased central sympathetic output to the heart, kidney and skeletal muscles.

    “In essential hypertension (EHT), the elevated arterial pressure has been associated with increased central sympathetic output to the heart, kidney and skeletal muscles (11–13).”

    From Hypertensive left ventricular hypertrophy: relation to peripheral sympathetic drive (2001) · cites this paper as [11]

  • The onset of hypertension is associated with sympathetic hyperactivity, while eventually the severity of hypertension is maintained, in part, by the occurrence of end-organ structural changes.

    “These findings have provided support to the theory that the onset of hypertension is associated with sympathetic hyperactivity, while, eventually, the severity of hypertension is maintained, in part, by the occurrence of end-organ structural changes (11,34).”

    From Hypertensive left ventricular hypertrophy: relation to peripheral sympathetic drive (2001) · cites this paper as [11]

  • Sympathetic activation in essential hypertension contributes to cardiovascular risk.

    “sympathetic activation in EHT is believed to contribute to cardiovascular risk.13,14”

    From Sympathetic Neural Activation in Nondiabetic Metabolic Syndrome and Its Further Augmentation by Hypertension (2004) · cites this paper as [13]

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Authors
JULIUS, S., & NESBITT, S.
Affiliations
University of Michigan (US)
Corresponding author
JULIUS, S
Venue
American Journal of Hypertension
Publisher
Oxford University Press (OUP)
Published
1996-11
Volume
9
Issue
11
Pages
113S-120S
ISSN
0895-7061 (ISSN-L)
DOI
10.1016/0895-7061(96)00287-7
OpenAlex
W1993942986
Semantic Scholar
03fca351e71d6b2381f8e1a352ac81fe79d5a4c3
Cited by
237
References
59
Citations by year
2026: 2 · 2025: 1 · 2024: 6 · 2023: 2 · 2022: 7 · 2021: 9 · 2020: 10 · 2019: 9 · 2018: 7 · 2017: 4 · 2016: 5 · 2015: 7 · 2014: 10 · 2013: 11 · 2012: 10
FWCI
3.77
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Hypertension (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r37hl037464-10)
  • National Heart, Lung, and Blood Institute (HL-37464)
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK20572)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Rate Variability and Autonomic Control
  • Health Sciences › Medicine › Surgery › Cardiovascular Syncope and Autonomic Disorders
Keywords
sympathetic hyperactivity, hypertension, autonomic dysfunction, neurogenic hypertension, white coat hypertension, metabolic syndrome, insulin resistance, dyslipidemia, coronary artery disease, platelet aggregation, hematocrit, central blood pressure regulation
MeSH terms
Animals, Humans, Hypertension, Sympathetic Nervous System

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