The pathophysiology of hypertension in patients with obesity
Open accessAbstract
The combination of obesity and hypertension is associated with high morbidity and mortality because it leads to cardiovascular and kidney disease. Potential mechanisms linking obesity to hypertension include dietary factors, metabolic, endothelial and vascular dysfunction, neuroendocrine imbalances, sodium retention, glomerular hyperfiltration, proteinuria, and maladaptive immune and inflammatory responses. Visceral adipose tissue also becomes resistant to insulin and leptin and is the site of altered secretion of molecules and hormones such as adiponectin, leptin, resistin, TNF and IL-6, which exacerbate obesity-associated cardiovascular disease. Accumulating evidence also suggests that the gut microbiome is important for modulating these mechanisms. Uric acid and altered incretin or dipeptidyl peptidase 4 activity further contribute to the development of hypertension in obesity. The pathophysiology of obesity-related hypertension is especially relevant to premenopausal women with obesity and type 2 diabetes mellitus who are at high risk of developing arterial stiffness and endothelial dysfunction. In this Review we discuss the relationship between obesity and hypertension with special emphasis on potential mechanisms and therapeutic targeting that might be used in a clinical setting.
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Activation of the renin-angiotensin-aldosterone system (RAAS) is a mediator of abnormal kidney function and increased blood pressure during development of obesity hypertension.
“2) activation of the renin-angiotensin-aldosterone system (RAAS)”
From Obesity-Induced Hypertension: Interaction of Neurohumoral and Renal Mechanisms (2015) · cites this paper as [37]
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Turak, O., Özcan, F., Tok, D., et al. (2012) · Journal of Clinical Hypertension · doi:10.1111/jch.12026 · Cited by 79 · see citing works
Aghamohammadzadeh, R., & Heagerty, A. M. (2012) · Annals of Medicine · doi:10.3109/07853890.2012.663928 · Cited by 78 · see citing works
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T-Cell Costimulation Protects Obesity-Induced Adipose Inflammation and Insulin Resistance
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Angiotensin II-dependent increased expression of Na + -glucose cotransporter in hypertension
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Vascular insulin resistance in prehypertensive rats: Role of PI3-kinase/Akt/eNOS signaling
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Obesity-Induced Hypertension: Interaction of Neurohumoral and Renal Mechanisms
Hall, J. E., do Carmo, J. M., da Silva, A. A., Wang, Z., & Hall, M. E. (2015) · Circulation Research · doi:10.1161/circresaha.116.305697 · Cited by 1,360 · see citing works
Obesity, kidney dysfunction and hypertension: mechanistic links
Hall, J. E., do Carmo, J. M., da Silva, A. A., Wang, Z., & Hall, M. E. (2019) · Nature Reviews Nephrology · doi:10.1038/s41581-019-0145-4 · Cited by 654 · see citing works
The Renin Angiotensin Aldosterone System in Obesity and Hypertension
Cabandugama, P. K., Gardner, M. J., & Sowers, J. R. (2017) · Medical Clinics of North America · doi:10.1016/j.mcna.2016.08.009 · Cited by 168 · see citing works
Self-citationOvernutrition, mTOR signaling, and cardiovascular diseases
Jia, G., Aroor, A. R., Martinez-Lemus, L. A., & Sowers, J. R. (2014) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00262.2014 · Cited by 122 · see citing works
Self-citationGut hormones and gut microbiota: implications for kidney function and hypertension
Afsar, B., Vaziri, N. D., Aslan, G., Tarim, K., & Kanbay, M. (2016) · Journal of the American Society of Hypertension · doi:10.1016/j.jash.2016.10.007 · Cited by 63 · see citing works
Huang, Y., Liu, Y., Ma, Y., Tu, T., Liu, N., Bai, F., Xiao, Y., Liu, C., Hu, Z., Lin, Q., et al. (2022) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2022.840866 · Cited by 54 · see citing works
- Authors
- DeMarco, V. G., Aroor, A. R., & Sowers, J. R.
- Affiliations
- University of Missouri (US)
- Corresponding author
- Sowers, James R.
- Venue
- Nature Reviews Endocrinology
- Published
- 2014-04-15
- Volume
- 10
- Issue
- 6
- Pages
- 364-376
- ISSN
- 1759-5029 (ISSN-L)
- 1759-5037
- PMC
- PMC4308954
- OpenAlex
- W2012416246
- Cited by
- 545
- References
- 239
- Citations by year
- 2026: 30 · 2025: 41 · 2024: 38 · 2023: 70 · 2022: 48 · 2021: 51 · 2020: 56 · 2019: 53 · 2018: 40 · 2017: 41 · 2016: 40 · 2015: 26 · 2014: 11
- FWCI
- 6.34
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- CYTED Ciencia y Tecnología para el Desarrollo
- National Institutes of Health (5r01hl107910-03)
- National Heart, Lung, and Blood Institute (R01 HL73101‑01A1, R01 HL 107910-01, R01-HL-107910, R01HL073101)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- obesity, obesity-related hypertension, pathophysiology, visceral adipose tissue, endothelial dysfunction, sodium retention, glomerular hyperfiltration, proteinuria, insulin resistance, leptin resistance, adiponectin, resistin, TNF-α, interleukin-6, gut microbiota, uric acid, incretins, dipeptidyl peptidase IV, arterial stiffness, premenopausal women, type 2 diabetes, cardiovascular disease, kidney disease
- MeSH terms
- Cardiotonic Agents, Diet, Humans, Hypertension, Life Style, Obesity
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.
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