Physiologic consequences of increased vascular oxidant stresses in hypercholesterolemia and atherosclerosis: Implications for impaired vasomotion
Abstract
During the past 8 years, it has become apparent that endothelium-dependent vascular relaxation is abnormal in a variety of disease states, including hypercholesterolemia, atherosclerosis, diabetes, hypertension, and following heart transplantation. Our laboratory and several others have examined dysfunctional regulation of vasomotor tone in hypercholesterolemia and atherosclerosis. These studies have led to the concepts that altered regulation of vasomotion by the endothelium (1) is an early development in atherosclerosis, (2) involves both large vessels (with overt atherosclerosis) and the microcirculation (in which atherosclerosis does not develop), and (3) can be reversed by lipid-lowering strategies. The mechanisms for the abnormalities underlying this form of endothelial dysfunction are likely multifactorial, but a major underlying factor appears to be increased oxidant degradation of endothelium-derived nitric oxide. In this review we examine the evidence supporting this conclusion and consider the implications of these findings.
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Excess superoxide or other ROS in the cell causes modification of different parts of the cellular machinery and is a known player in the genesis and progression of cardiovascular disease.
“The excess of superoxide, or other ROS, in the cell causes the modification of different parts of the cellular machinery and is a known player in the genesis and progression of cardiovascular disease (227, 408, 409, 570, 672, 700, 893).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [409]
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- Authors
- Harrison, D. G., & Ohara, Y.
- Affiliations
- Emory University (US)
- Corresponding author
- Harrison, David G.
- ORCID
- Harrison, David G.
- Venue
- The American Journal of Cardiology
- Publisher
- Elsevier BV
- Published
- 1995-02
- Volume
- 75
- Issue
- 6
- Pages
- 75B-81B
- ISSN
- 0002-9149 (ISSN-L)
- OpenAlex
- W2061679479
- Cited by
- 163
- References
- 41
- Citations by year
- 2025: 2 · 2024: 1 · 2023: 5 · 2022: 1 · 2021: 5 · 2020: 2 · 2019: 2 · 2018: 2 · 2017: 2 · 2016: 2 · 2015: 2 · 2014: 3 · 2013: 1 · 2012: 1
- FWCI
- 2.15
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The American Journal of Cardiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01hl037217-05)
- National Heart, Lung, and Blood Institute (R01HL039006, HL37217, HL-15696, HL-39006)
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Keywords
- endothelial dysfunction, hypercholesterolemia, atherosclerosis, oxidative stress, nitric oxide degradation, endothelium-dependent vasodilation, vascular tone, lipid-lowering therapy, microcirculation, large arteries
- MeSH terms
- Animals, Arteriosclerosis, Endothelium, Vascular, Humans, Hypercholesterolemia, Nitric Oxide, Stress, Physiological, Superoxides, Vasomotor System
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