Autonomic Contribution to Blood Pressure and Metabolism in Obesity
Abstract
Obesity is associated with alterations in the autonomic nervous system that may contribute to the increase in blood pressure and resting energy expenditure present in this condition. To test this hypothesis, we induced autonomic withdrawal with the ganglionic blocker trimethaphan in 10 lean (32±3 years) and 10 obese (35±3 years) subjects. Systolic blood pressure fell more in obese compared with lean subjects (−17±3 versus −11±1 mm Hg; P =0.019) because of a greater decrease in total peripheral resistance (−310±41 versus 33±78 dynes/sec/cm −5 ; P =0.002). In contrast, resting energy expenditure decreased less in obese than in lean subjects, (−26±21 versus −86±15 kcal per day adjusted by fat-free mass; P =0.035). We confirmed that the autonomic contribution to blood pressure was greater in obesity after including additional subjects with a wider range of blood pressures. Systolic blood pressure decreased −28±4 mm Hg (95% CI: −38 to −18.0; n=8) in obese hypertensive subjects compared with lean (−9±1 mm Hg; 95% CI: −11 to −6; n=22) or obese normotensive subjects (−14±2 mm Hg; 95% CI: −18 to −10; n=20). After removal of autonomic influences, systolic blood pressure remained higher in obese hypertensive subjects (109±3 versus 98±2 mm Hg in lean and 103±2 mm Hg in obese normotensive subjects; P =0.004) suggesting a role for additional factors in obesity-associated hypertension. In conclusion, sympathetic activation induced by obesity is an important determinant to the blood pressure elevation associated with this condition but is not effective in increasing resting energy expenditure. These results suggest that the sympathetic nervous system could be targeted in the treatment of obesity-associated hypertension.
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After ganglionic blockade, blood pressure was normalized in obese normotensives, while in obese hypertensives it decreased but did not completely normalize, indicating that factors other than the sympathetic nervous system contribute to obesity-associated hypertension.
“Third, after ganglionic blockade, blood pressure was normalized in the obese normotensives. Blood pressure also decreased in the obese hypertensives but it did not completely indicating that factors other than the sympathetic nervous system contribute to obesity-associated hypertension.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [69]
The fall in blood pressure with ganglionic blockade in obese hypertensives was double that in obese normotensives, consistent with an important role for the sympathetic nervous system in maintaining blood pressure in obese hypertensives.
“Second, the fall in blood pressure with ganglionic blockade in the obese hypertensives was double that in the obese normotensives, consistent with an important role for the sympathetic nervous system in maintaining blood pressure in obese hypertensives.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [69]
Ganglionic blockade produced an exaggerated fall in vascular resistance and blood pressure in obese compared with lean normotensive subjects.
“First, ganglionic blockade produced an exaggerated fall in vascular resistance and blood pressure in obese compared with lean normotensive subjects.”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [69]
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- Authors
- Shibao, C., Gamboa, A., Diedrich, A., Ertl, A. C., Chen, K. Y., Byrne, D. W., Farley, G., Paranjape, S. Y., Davis, S. N., & Biaggioni, I.
- Affiliations
- Vanderbilt University (US)
- From the Division of Clinical Pharmacology and the Autonomic Dysfunction Center (C.S., A.G., A.D., G.F., S.Y.P., I.B.) and Divisions of Gastroenterology (K.Y.C.) and Diabetes, Endocrinology, and Metabolism (A.C.E., S.N.D.), Department of Medicine, and the Department of Biostatistics and the General Clinical Research Center (D.W.B.), Vanderbilt University School of Medicine, Nashville, Tenn.
- ORCID
- Venue
- Hypertension
- Published
- 2007-01
- Volume
- 49
- Issue
- 1
- Pages
- 27-33
- ISSN
- 0194-911X (ISSN-L)
- 1524-4563
- OpenAlex
- W2137064396
- Cited by
- 147
- References
- 45
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 5 · 2023: 5 · 2022: 6 · 2021: 7 · 2020: 4 · 2019: 5 · 2018: 5 · 2017: 9 · 2016: 12 · 2015: 9 · 2014: 12 · 2013: 9 · 2012: 9
- FWCI
- 6.43
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Hypertension (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (HL56693, P01HL056693)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK 20593)
- National Center for Research Resources (M01RR000095, M01-RR-00095)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Rate Variability and Autonomic Control
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
- Keywords
- obesity, obesity-related hypertension, autonomic nervous system, sympathetic nervous system, trimethaphane, ganglionic blockade, blood pressure, resting energy expenditure, systemic vascular resistance, sympathetic activation
- MeSH terms
- Adult, Autonomic Nervous System, Blood Pressure, Cardiovascular System, Energy Metabolism, Female, Ganglionic Blockers, Humans, Hypertension, Male, Obesity, Rest, Systole, Thinness, Trimethaphan, Vascular Resistance
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