Hypercholesterolemia promotes inflammation and microvascular dysfunction: role of nitric oxide and superoxide1
| Autor: | Karen Y. Stokes, Dianne Cooper, D. Neil Granger, Anitaben Tailor |
|---|---|
| Rok vydání: | 2002 |
| Předmět: |
chemistry.chemical_classification
Reactive oxygen species Endothelium Superoxide Ischemia Inflammation Pharmacology medicine.disease Biochemistry Nitric oxide Proinflammatory cytokine Microcirculation chemistry.chemical_compound medicine.anatomical_structure chemistry Physiology (medical) Immunology medicine medicine.symptom |
| Zdroj: | Free Radical Biology and Medicine. 33:1026-1036 |
| ISSN: | 0891-5849 |
| Popis: | Relatively brief periods (days) of hypercholesterolemia can exert profound effects on endothelium-dependent functions of the microcirculation, including dilation of arterioles, fluid filtration across capillaries, and regulation of leukocyte recruitment in postcapillary venules. Hypercholesterolemia appears to convert the normal anti-inflammatory phenotype of the microcirculation to a proinflammatory phenotype. This phenotypic change appears to result from a decline in nitric oxide (NO) bioavailability that results from a reduction in NO biosynthesis, inactivation of NO by superoxide (O(2)(*)(-)), or both. A consequence of the hypercholesterolemia-induced microvascular responses is an enhanced vulnerability of the microcirculation to the deleterious effects of ischemia and other inflammatory conditions. Hence, therapeutic strategies that are directed towards preventing the early microcirculatory dysfunction and inflammation caused by hypercholesterolemia may prove effective in reducing the high mortality associated with ischemic tissue diseases. Agents that act to maintain the normal balance between NO and reactive oxygen species (ROS) in vascular endothelial cells may prove particularly useful in this regard. |
| Databáze: | OpenAIRE |
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