Clinical and experimental pharmacology & physiology
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Clin. Exp. Pharmacol. Physiol. · Nov 2008
ReviewSuppressing NADPH oxidase-dependent oxidative stress in the vasculature with nitric oxide donors.
1. Reactive oxygen species produced in the vasculature, including superoxide anion, contribute to the pathogenesis of cardiovascular disease states, such as atherosclerosis. A critical source of superoxide is vascular NADPH oxidase and upregulation of this enzyme brings about the oxidative stress underlying atherosclerosis. ⋯ These problems of nitrates have not only limited their therapeutic exploitation, but have also stifled interest in newer-generation NO donors. 3. Recent evidence indicates that, in stark contrast with the organic nitrates, the newer-age diazeniumdiolate NONOate class of NO donors suppress vascular NADPH oxidase-dependent superoxide production and are less likely to induce tolerance, making them more suitable for suppression of oxidative stress in atherosclerosis. 4. Here, it is hypothesized that NONOates provide a novel means of suppressing NADPH oxidase-dependent oxidative stress to restore vascular NO levels to prevent, and even reverse, atherosclerosis.
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Clin. Exp. Pharmacol. Physiol. · Nov 2008
Comparative StudySpinal mu-opioid receptor expression and hyperalgesia with dexamethasone in chronic adjuvant-induced arthritis in rats.
1. It is known that inflammation influences peripheral and central mu-opioid receptor expression. Previous studies have indicated that glucocorticoids may influence the density of mu-opioid receptors. ⋯ The AA + dexamethasone group showed a significant decrease in hyperalgesia on Day 6 compared with the AA group, but hyperalgesia increased significantly on Day 21 in the AA + dexamethasone group compared with the AA group. 4. The effects of long-term dexamethasone on both spinal mu-opioid receptor expression and hyperalgesia during persistent AA inflammation are time dependent. In addition, the effect of long-term dexamethasone administration on hyperalgesia during persistent arthritis inflammation needs to be investigated further.