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Endothelial cells, lining all blood vessels, contain the enzyme nitric oxide synthase (eNOS), which catalyzes the release of nitric oxide (NO) from various substrates. Vascular endothelial-derived NO is critical to maintaining the vasodilator tone essential for the regulation of blood flow and pressure. Up-regulation of eNOS in these cells results in enhanced vasodilation and concomitant increase in blood flow. Any condition characterized by reduction in blood flow, therefore, should benefit by therapies which would reverse or offset decreased blood flow. Cardiovascular Applications HMG CoA reductase inhibitors (statins) have been shown to improve endothelium-dependent vasodilation in both coronary and peripheral arteries, independent of their lipid lowering effects. Enhancement of eNOS production results in increased coronary endothelial NO production that enhances NO-dependent coronary vasodilation and NO-mediated regulation of myocardial oxygen consumption, to yield improved blood flow and increased endothelial function. eNOS Pharmaceuticals' drug candidates are designed to increase eNOS production. This results in improved vasodilator response and increased endothelial function. These physiological changes in turn improve blood flow to ischemic tissue and reduce or limit the tissue injury associated with many cardiovascular diseases. Alzheimer's Disease Applications Advancing age is closely associated with certain physiologic changes, among them changes in the vascular system including clogging of arteries and hardening and thickening of blood vessel walls. Along with this increase in vascular stenosis is a decrease in cerebral blood flow. Increased vascular stenosis is frequently closely associated with the decreasing cognitive status found in Alzheimer's disease. Use of eNOS Pharmaceuticals' therapeutics could slow the progression of AD by maintaining blood vessel elasticity, thereby delaying vascular stenosis. Ischemic Stroke Applications Stroke occurs when blood flow to the brain is interrupted by a blocked or burst artery. This sudden decrease in blood flow to a specific area of the brain deprives brain cells of oxygen and other nutrients. Ischemia develops and brain cells within the core die. Brain cells surrounding the core, a region called the penumbra, do not suffer immediate, irreversible effects. They are temporarily neurologically and electrically impaired. Restoration of cerebral blood flow, even to suboptimal levels, provides an opportunity for these cells to recover and regain functionality. |
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