Obesity-Induced Hypertension: New Concepts From the Emerging Biology of Obesity
Abstract
Abstract —Obesity is associated with an increased risk of hypertension. In the past 5 years there have been dramatic advances into the genetic and neurobiological mechanisms of obesity with the discovery of leptin and novel neuropeptide pathways regulating appetite and metabolism. In this brief review, we argue that these mounting advances into the neurobiology of obesity have and will continue to provide new insights into the regulation of arterial pressure in obesity. We focus our comments on the sympathetic, vascular, and renal mechanisms of leptin and melanocortin receptor agonists and on the regulation of arterial pressure in rodent models of genetic obesity. We suggest 3 concepts. First, the effect of obesity on blood pressure may depend critically on the genetic-neurobiological mechanisms underlying the obesity. Second, obesity is not consistently associated with increased blood pressure, at least in rodent models. Third, the blood pressure response to obesity may be critically influenced by modifying alleles in the genetic background.
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The effect of obesity on blood pressure may depend critically on the genetic-neurobiologic mechanisms underlying the obesity.
“First, the effect of obesity on blood pressure may depend critically on the genetic-neurobiologic mechanisms underlying the obesity.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [78]
Obesity is not consistently associated with increased blood pressure.
“Second, obesity is not consistently associated with increased blood pressure.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [78]
The genetic neurobiologic basis of obesity can critically influence the sympathetic and blood pressure response to obesity, and hypothalamic melanocortin-4 receptors contribute to regulation of sympathetic activity and blood pressure in obese humans.
“These data support the concept, discussed above, that the genetic neurobiologic basis of obesity can critically influence the sympathetic and blood pressure response to obesity78, and demonstrate that hypothalamic melanocortin-4 receptors contribute to regulation of sympathetic activity and blood pressure in obese humans.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [78]
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- Authors
- Mark, A. L., Correia, M., Morgan, D. A., Shaffer, R. A., & Haynes, W. G.
- Affiliations
- University of Iowa (US)
- Venue
- Hypertension
- Published
- 1999-01
- Volume
- 33
- Issue
- 1
- Pages
- 537-541
- ISSN
- 0194-911X (ISSN-L)
- 1524-4563
- OpenAlex
- W2081593602
- Cited by
- 185
- References
- 33
- Citations by year
- 2024: 1 · 2023: 2 · 2022: 1 · 2021: 3 · 2019: 5 · 2017: 8 · 2016: 4 · 2015: 1 · 2014: 6 · 2013: 9 · 2012: 4
- FWCI
- 1.84
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Hypertension (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5p50hl044546-05, 5r29hl043514-05)
- National Heart, Lung, and Blood Institute (HL-43514, HL-55006, HL-44546, P50HL055006)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Keywords
- obesity, leptin, melanocortin receptor agonist, sympathetic nervous system, renal mechanisms, vascular mechanisms, blood pressure regulation, genetic obesity model, appetite regulation, genetic background, rodent models
- MeSH terms
- Animals, Appetite, Carrier Proteins, Humans, Hypertension, Neuropeptides, Obesity, Proteins, Receptors, Cell Surface, Risk Factors, Receptors, Corticotropin, Leptin, Receptor, Melanocortin, Type 4, Receptors, Leptin
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