Differing Pattern of Sympathoexcitation in Normal-Weight and Obesity-Related Hypertension
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Hypertension in normal-weight and obese individuals is characterized by activation of the sympathetic nervous system. Measurement of spillover of the sympathetic transmitter, norepinephrine, to plasma indicates that the regional pattern of sympathetic activation in the 2 “variants” of essential hypertension differs, excluding the heart in obesity-related hypertension. Whether sympathetic nerve firing characteristics also differ is unknown. We studied multiunit and single fiber sympathetic nerve firing properties in patients with normal-weight hypertension and obesity-related hypertension, comparing these with nerve characteristics in normal-weight and obese people with normal blood pressure. Both normal-weight hypertensive (n=10) and obese hypertensive (n=14) patients had increased total multiunit muscle sympathetic nerve activity compared with the normal-weight (n=11) and obese (n=11) people with normal blood pressure (65±4 versus 47±6 bursts per 100 heartbeats, P <0.01 in the normal-weight groups and 68±4 versus 53±3 bursts per 100 beats, P <0.01 in the obese groups). Sympathetic activation in normal-weight hypertension was characterized by increased firing rate of single vasoconstrictor fibers (70±8 versus 28±3 spikes per 100 beats; P <0.001), increased firing probability per heartbeat (39±3% versus 20±3%; P <0.001), and higher incidence of multiple spikes per heartbeat (30±4% versus 17±4%; P <0.05). Sympathetic activation in obesity-related hypertension differed, involving recruitment of previously silent fibers, which fired at a normal rate. The pattern of sympathetic activation in normal-weight and obesity-related hypertension differs in terms of both the firing characteristics of individual sympathetic fibers and the sympathetic outflows involved. The underlying central nervous system mechanism and the adverse consequences of the 2 modes of sympathetic activation may differ.
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In lean hypertensive patients, the increase in sympathetic activity evident in multiunit burst number and size is because of an increase in the firing rate of individual single fibers and to the common presence of firing salvos, multiple firings in a single cardiac cycle.
“In lean hypertensive patients, the increase in sympathetic activity evident in multiunit burst number and size is because of an increase in the firing rate of individual single fibers, and to the common presence of firing salvos, multiple firings in a single cardiac cycle 31 (Figure 2).”
From Obesity Paradox in Hypertension: Is This Because Sympathetic Activation in Obesity-Hypertension Takes a Benign Form? (2018) · cites this paper as [31]
Multiunit sympathetic nerve firing is similarly increased in both lean and obese hypertensive patients.
“That multiunit sympathetic nerve firing is similarly increased in both lean and obese hypertensive patients is well known.31,32”
From Obesity Paradox in Hypertension: Is This Because Sympathetic Activation in Obesity-Hypertension Takes a Benign Form? (2018) · cites this paper as [31]
With the coexistence of impaired norepinephrine reuptake with firing salvos in normal-weight essential hypertension and in depressive illness and panic disorder, there is evidence of cardiac risk, even in panic disorder.
“Conversely, with the coexistence of impaired norepinephrine reuptake with firing salvos in normal-weight essential hypertension 31,[33][34][35][36] and in depressive illness 42,51,79 and panic disorder, 51,79,80 there is evidence of cardiac risk, 84 even in panic disorder.[85][86][87]”
From Obesity Paradox in Hypertension: Is This Because Sympathetic Activation in Obesity-Hypertension Takes a Benign Form? (2018) · cites this paper as [31]
In obese hypertensive humans, there is enhanced muscle sympathetic nerve activity, but the neurophysiologic basis of this increase is different in obese vs lean hypertensive subjects.
“In obese hypertensive humans, there is enhanced muscle sympathetic nerve activity, but the neurophysiologic basis of this increase is different in obese vs lean hypertensive subjects67.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [67]
In lean hypertensive patients, the increased sympathetic activity is related to increased firing frequency of single nerve fibers.
“In lean hypertensive patients, the increased sympathetic activity is related to increased firing frequency of single nerve fibers.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [67]
In obese normotensive and hypertensive subjects, the increased sympathetic activity is due to recruitment of additional fibers and not to increasing firing frequency of single nerve fibers.
“In contrast, in obese normotensive and hypertensive subjects, the increased activity is due to recruitment of additional fibers and not to increasing firing frequency of single nerve fibers67.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [67]
A prohypertensive contribution of increased muscle sympathetic nerve activity, which is higher in hypertensive vs normotensive obese humans, is the most likely explanation for the seemingly conflicting observations about renal norepinephrine spillover and sympathetic contribution to blood pressure.
“The most likely is a prohypertensive contribution of increased muscle sympathetic nerve activity which is higher in hypertensive vs normotensive obese humans67.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [67]
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Self-citationCafeteria Diet Increases Fat Mass and Chronically Elevates Lumbar Sympathetic Nerve Activity in Rats
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Self-citationObesity-Associated Organ Damage and Sympathetic Nervous Activity
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Self-citationGallina, S., Mauro, M. D., D’Amico, M. A., D’Angelo, E., Sablone, A., Fonso, A. D., Bascelli, A., Izzicupo, P., & Baldassarre, A. D. (2011) · Clinical Endocrinology · doi:10.1111/j.1365-2265.2011.04143.x · Cited by 57 · see citing works
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Esler, M., Lambert, G. W., Esler, D., Sari, C. I., Guo, L. J., & Jennings, G. (2020) · Journal of Hypertension · doi:10.1097/hjh.0000000000002407 · Cited by 57 · see citing works
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Self-citationSex Differences in Renal Inflammation and Injury in High-Fat Diet–Fed Dahl Salt-Sensitive Rats
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Altered regulation of the rostral ventrolateral medulla in hypertensive obese Zucker rats
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The Role of Beta-Blockers in the Treatment of Hypertension
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Neuroadrenergic dysfunction in obesity: an overview of the effects of weight loss
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Self-citationBurke, P. G. R., Li, Q., Costin, M. L., McMullan, S., Pilowsky, P. M., & Goodchild, A. K. (2008) · Hypertension · doi:10.1161/hypertensionaha.108.118224 · Cited by 46 · see citing works
Murai, H., Takamura, M., Maruyama, M., Nakano, M., Ikeda, T., Kobayashi, D., Otowa, K., Ootsuji, H., Okajima, M., Furusho, H., et al. (2009) · The Journal of Physiology · doi:10.1113/jphysiol.2009.172627 · Cited by 46 · see citing works
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Autonomic Function in Hypertension
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Lambert, E., Dawood, T., Schlaich, M., Straznicky, N., Esler, M., & Lambert, G. (2008) · Clinical and Experimental Pharmacology and Physiology · doi:10.1111/j.1440-1681.2008.04905.x · Cited by 44 · see citing works
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Autonomic Nervous System Function in Anorexia Nervosa: A Systematic Review
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Self-citationImpact of sex and age on metabolism, sympathetic activity, and hypertension
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Sympathetic neural mechanisms in human hypertension
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Factors Responsible for Obesity-Related Hypertension
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Central mechanisms in sympathetic nervous dysregulation in obesity
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Sympathetic activity in obesity: a brief review of methods and supportive data
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Pathophysiology of Hypertension
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Peripheral Blood Flow Regulation in Human Obesity and Metabolic Syndrome
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Sympathetic Neural Control in Humans with Anxiety‐Related Disorders
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Sympathetic Pathophysiology in Hypertension Origins: The Path to Renal Denervation
Esler, M., Osborn, J. W., & Schlaich, M. P. (2024) · Hypertension · doi:10.1161/hypertensionaha.123.21715 · Cited by 25 · see citing works
Self-citation
- Authors
- Lambert, E., Straznicky, N., Schlaich, M., Esler, M., Dawood, T., Hotchkin, E., & Lambert, G.
- Affiliations
- From the Human Neurotransmitters Laboratory, Baker Heart Research Institute, Melbourne, Victoria, Australia.
- Baker Heart and Diabetes Institute (AU)
- Venue
- Hypertension
- Published
- 2007-11
- Volume
- 50
- Issue
- 5
- Pages
- 862-868
- ISSN
- 0194-911X (ISSN-L)
- 1524-4563
- OpenAlex
- W2168053032
- Cited by
- 195
- References
- 41
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 6 · 2023: 4 · 2022: 3 · 2021: 8 · 2020: 9 · 2019: 14 · 2018: 6 · 2017: 14 · 2016: 17 · 2015: 14 · 2014: 12 · 2013: 11 · 2012: 13
- FWCI
- 9.57
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Hypertension (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Diabetes Australia
- Medical Research Council
- National Health and Medical Research Council (225108)
- 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 › Complementary and alternative medicine › Cardiovascular and exercise physiology
- Keywords
- obesity-related hypertension, sympathetic activation, muscle sympathetic nerve activity, norepinephrine spillover, firing probability, sympathetic outflow, essential hypertension
- MeSH terms
- Action Potentials, Adult, Aged, Blood Pressure, Electrocardiography, Electrophysiology, Female, Heart Rate, Humans, Hypertension, Male, Microelectrodes, Middle Aged, Obesity, Peroneal Nerve, Sympathetic Nervous System, Thinness, Sympathetic Fibers, Postganglionic
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