Effect of obesity on endothelium-dependent, nitric oxide-mediated vasodilation in normotensive individuals and patients with essential hypertension
Abstract
The purpose of this study was to determine the interdependent and independent effects of hypertension and obesity on endothelial function in humans. We evaluated the forearm blood flow (FBF) response to acetylcholine, an endothelium-dependent vasodilator, and isosorbide dinitrate (ISDN), an endothelium-independent vasodilator, in 16 lean and 12 obese normotensive individuals and the 18 lean and 15 obese hypertensive patients with no history of smoking, hypercholesterolemia, diabetes mellitus, or renal dysfunction. The FBF was measured using a mercury-filled Silastic strain-gauge plethysmograph. The systolic and diastolic blood pressures (BP) and forearm vascular resistance were significantly greater in hypertensive patients than in the normotensive individuals. Insulin resistance, determined by a homeostatic model assessment (HOMA), was significantly greater in the obese group than in the lean group (3.59 +/- 1.68 v 1.91 +/- 1.12, P < .01). There was no significant difference in the HOMA index between normotensive and hypertensive subjects regardless of weight. The response of FBF to acetylcholine was greatest in lean normotensive individuals and least in obese hypertensive patients (40.5 +/- 8.5 and 10.4 +/- 2.8 mL/min/100 mL of tissue, P < .001 v other groups). The FBF response was similar in obese normotensive individuals and lean hypertensive patients (24.1 +/- 7.9 and 19.3 +/- 3.2 mL/min/100 mL of tissue). The vasodilatory effect of ISDN was similar in all four groups. Multiple regression analysis revealed that the maximal FBF response to acetylcholine correlated independently with age (P = .043), obesity (P = .012), HOMA index (P = .002), and mean BP (P < .001). These findings suggest that obesity and hypertension are independently involved in abnormal endothelium-dependent vasodilation by attenuated nitric oxide production.
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NO bioavailability is decreased in animal models of diet-induced obesity and in obese and insulin-resistant patients.
“NO bioavailability is decreased in animal models of diet-induced obesity and in obese and insulin resistant patients”
From Regulation of obesity and insulin resistance by nitric oxide (2014) · cites this paper as [118]
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- Authors
- Higashi, Y.
- Affiliations
- Hiroshima University (JP)
- Corresponding author
- Higashi, Y
- ORCID
- Higashi, Y
- Venue
- American Journal of Hypertension
- Publisher
- Oxford University Press (OUP)
- Published
- 2001-10
- Volume
- 14
- Issue
- 10
- Pages
- 1038-1045
- ISSN
- 0895-7061 (ISSN-L)
- OpenAlex
- W2012569482
- Cited by
- 125
- References
- 36
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 3 · 2023: 2 · 2022: 3 · 2021: 6 · 2020: 6 · 2019: 3 · 2018: 3 · 2017: 6 · 2016: 7 · 2015: 7 · 2014: 7 · 2013: 2 · 2012: 3
- FWCI
- 3.90
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Hypertension (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Pfizer
- Japan Heart Foundation
- Kimura Memorial Heart Foundation
- Pfizer Pharmaceuticals
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
- Keywords
- obesity, essential hypertension, endothelial function, nitric oxide, endothelium-dependent vasodilation, acetylcholine, isosorbide dinitrate, forearm blood flow, insulin resistance, HOMA index, forearm vascular resistance, age
- MeSH terms
- Acetylcholine, Adult, Endothelium, Vascular, Female, Humans, Hypertension, Isosorbide Dinitrate, Male, Middle Aged, Nitric Oxide, Obesity, Vasodilation, Vasodilator Agents, Body Mass Index
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