Increasing evidence implicates the role of reactive oxygen species in the pathogenesis of several diseases such as cardiovascular disease. Recent studies also suggest a role for reactive oxygen species in the control of vascular smooth muscle proliferation both in vitro and in vivo. By altering the balance in the endothelium between vasoconstrictors such as thromboxane, isoprostanes and vasodilators such as nitric oxide, reactive oxygen species contribute to endothelium-dependent contractions and increased vascular resistance. Studies in animal models of atherosclerosis suggest that natural and synthetic antioxidants can retard the development of atheroma. Antioxidants can restore endothelial function and decrease blood pressure in several models of hypertension and in some essential hypertension of humans. Epidemiological comparisons between populations and studies within populations also support the contention that high plasma levels or dietary intake of natural antioxidant may protect against the development of coronary disease in man. Endothelial dysfunction is increasingly recognized as an early event in the pathogenesis of cardiovascular disease. Endothelial dysfunction and coronary artery diseases are both linked to hypertension. Modification of these conditions improves both endothelial function and coronary artery disease outcomes. Dietary and lifestyle modifications and antioxidant vitamin supplementation have a beneficial effect on endothelial function, as do angiotensin-converting enzyme inhibitors and lipid-lowering agents. Oxidative stress increases cell proliferation, mediates hormone-induced hypertrophy, and under some circumstances-induces apoptosis. Smooth muscle cells contain a reduced nicotinamide adenine dinucleotide/reduced nicotinamide adenine dinucleotide phosphate oxidase that is responsible for the majority of the superoxide produced by the vessel wall. This enzyme has been characterized biochemically, but only limited information is available regarding its molecular structure. High levels of oxidative stress are apparently involved in the pathogenesis of vascular diseases such as hypertension and atherosclerosis. Thus the pathways responsible for oxidative stress, as well as the antioxidant defenses in the vessel wall, may provide novel therapeutic targets.
| Identifer | oai:union.ndltd.org:arizona.edu/oai:arizona.openrepository.com:10150/289153 |
| Date | January 2000 |
| Creators | Hosseini, Saeed |
| Contributors | Watson, Ronald R. |
| Publisher | The University of Arizona. |
| Source Sets | University of Arizona |
| Language | en_US |
| Detected Language | English |
| Type | text, Dissertation-Reproduction (electronic) |
| Rights | Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author. |
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