Obesity-induced Hypertension: Role of Sympathetic Nervous System, Leptin, and Melanocortins
Open accessAbstract
Excess weight gain contributes to increased blood pressure in most patients with essential hypertension. Although the mechanisms of obesity hypertension are not fully understood, increased renal sodium reabsorption and impaired pressure natriuresis play key roles. Several mechanisms contribute to altered kidney function and hypertension in obesity, including activation of the sympathetic nervous system, which appears to be mediated in part by increased levels of the adipocyte-derived hormone leptin, stimulation of pro-opiomelanocortin neurons, and subsequent activation of central nervous system melanocortin 4 receptors.
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Leptin increases sympathetic nerve activity by binding to leptin receptors in the central nervous system and contributes to obesity-induced hypertension.
“In addition to regulating energy stores, leptin increases sympathetic nerve activity (SNA) by binding to leptin receptors (LepRs) in the CNS and contributes to obesity-induced hypertension6,121,122.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [121]
The role of the sympathetic nervous system in linking obesity with elevated blood pressure has been well documented in experimental models and in humans.
“The role of the SNS in linking obesity with elevated BP has been well documented in experimental models and in humans121,152.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [121]
Some rodent models of obesity, such as those with MC4R or leptin gene mutations, have normal or reduced SNS activity and decreased BP despite inflammation, insulin resistance, dyslipidemia, and other metabolic changes associated with obesity.
“Therefore, some rodent models of obesity, such as those with melanocortin 4 receptor (MC4R) or leptin gene mutations, have normal or reduced SNS activity and decreased BP despite inflammation, insulin resistance, dyslipidemia, and other metabolic changes associated with obesity17.”
From Obesity-Induced Hypertension: Interaction of Neurohumoral and Renal Mechanisms (2015) · cites this paper as [17]
Obesity generally decreases parasympathetic tone and increases sympathetic activity.
“Obesity generally decreases parasympathetic tone and increases sympathetic activity.”
From Obesity-Induced Hypertension: Interaction of Neurohumoral and Renal Mechanisms (2015) · cites this paper as [17]
Leptin and the CNS POMC pathway appear to be important in obesity-induced SNS activation and hypertension.
“Although the role of many of these factors is still uncertain, leptin and the CNS POMC pathway appear to be important in obesity-induced SNS activation and hypertension17,80–82.”
From Obesity-Induced Hypertension: Interaction of Neurohumoral and Renal Mechanisms (2015) · cites this paper as [17]
The melanocortin system also plays an important role in regulating sympathetic nervous system activity and blood pressure besides its effects on food intake and body weight regulation.
“Besides its effects on food intake and body weight regulation, the melanocortin system also plays an important role in regulating SNS activity and BP.”
From Role of the brain melanocortins in blood pressure regulation (2017) · cites this paper as [9]
Melanocortins play an important role in regulating blood pressure and sympathetic nervous system activity as well as energy balance, glucose and other metabolic functions in humans and experimental animals.
“Melanocortins play an important role in regulating blood pressure (BP) and sympathetic nervous system (SNS) activity as well as energy balance, glucose and other metabolic functions in humans and experimental animals.”
From Role of the brain melanocortins in blood pressure regulation (2017) · cites this paper as [9]
MC4R, activated mainly by α-MSH, is believed to be the key component of the brain melanocortin system's effects on sympathetic nervous system activation and blood pressure regulation.
“Although MC3Rs have been implicated in body weight regulation (mainly via effects on enery expenditure) and in preventing salt sensitivty of BP as previously discussed [22], MC4R, activated mainly by α-MSH, is believed to be the key component of the brain melanocortin system’s effects on SNS activation and BP regulation [9, 29, 30].”
From Role of the brain melanocortins in blood pressure regulation (2017) · cites this paper as [9]
Increased sympathetic nervous system activity mediates a major component of the increased blood pressure associated with obesity.
“Increased SNS activity mediates a major component of the increased BP associated with obesity [9, 43, 44].”
From Role of the brain melanocortins in blood pressure regulation (2017) · cites this paper as [9]
Leptin contributes to sympathetic overactivity and hypertension in a number of animal models of monogenic and diet-induced obesity.
“A large body of evidence has demonstrated that leptin contributes to sympathetic overactivity and hypertension in a number of animal models of monogenic and diet-induced obesity74–77.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [75]
Rodents with loss of function mutations in hypothalamic melanocortin-4 receptors are obese but lack sympathetic activation and obesity-associated hypertension.
“Rodents with loss of function mutations in the hypothalamic melanocortin-4 receptors are obese but lack sympathetic activation and obesity-associated hypertension74,75.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [75]
Stimulation of hypothalamic melanocortin-4 receptors increases sympathetic activity and blood pressure.
“In addition to inhibiting appetite and increasing metabolism, stimulation of hypothalamic melanocortin-4 receptors increases sympathetic activity and blood pressure74,75.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [75]
The brain melanocortin pathway is crucial in the regulation of sympathetic activity and blood pressure in obesity.
“The brain melanocortin pathway has emerged from studies in both experimental animals74,75 and humans89,90 as a crucial pathway in the regulation of sympathetic activity and BP in obesity.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [75]
The melanocortin system has a powerful influence on energy homeostasis and is critically involved in mediating the metabolic, sympathetic and cardiovascular effects of leptin and insulin.
“The melanocortin system has a powerful influence on energy homeostasis and is critically involved in mediating the metabolic, sympathetic and cardiovascular effects of leptin and insulin (32–35).”
From Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis (2014) · cites this paper as [32]
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- Authors
- Hall, J. E., da Silva, A. A., do Carmo, J. M., Dubinion, J., Hamza, S., Munusamy, S., Smith, G., & Stec, D. E.
- Affiliations
- University of Mississippi Medical Center (US)
- Corresponding author
- Hall, John E.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2010-06
- Volume
- 285
- Issue
- 23
- Pages
- 17271-17276
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC2878489
- OpenAlex
- W2072206476
- Cited by
- 528
- References
- 37
- Citations by year
- 2026: 15 · 2025: 17 · 2024: 45 · 2023: 24 · 2022: 19 · 2021: 20 · 2020: 39 · 2019: 39 · 2018: 31 · 2017: 36 · 2016: 49 · 2015: 42 · 2014: 54 · 2013: 33 · 2012: 36
- FWCI
- 5.17
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Heart Association (P01 HL51971, HL51971)
- National Institutes of Health (HL-51971)
- National Heart, Lung, and Blood Institute (P01-HL-51971, HL‐51971, P01HL051971)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- obesity-related hypertension, essential hypertension, sympathetic nervous system, leptin, melanocortin-4 receptor, proopiomelanocortin neurons, renal sodium reabsorption, pressure natriuresis, renal function, adipokines
- MeSH terms
- Adipose Tissue, Animals, Body Weight, Humans, Hypertension, Kidney, Models, Biological, Neurons, Obesity, Pro-Opiomelanocortin, Sympathetic Nervous System, Adipocytes, Leptin, Receptor, Melanocortin, Type 4, Mice, Rats, Melanocortins
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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