| Summary: | Increased sympathetic activity, due to stressful events, leads to chronically increased release of catecholamines from the sympathetic nervous system, resulting in deleterious effects on cardiac cells. Oxidative stress, due to excessive catecholamine release, affects the calcium handling ability of cardiomyocytes. It is believed that excess catecholamines exert cardiotoxic effects primarily via binding to adrenoceptors and causing intracellular calcium overload. However, excess catecholamines have additional influences that are linked to their chemical structure and sensitivity to oxidation. Catecholamines are known to undergo oxidation to generate free radicals, which are highly toxic, and in turn effect the calcium handling ability of cardiomyocytes and consequently, there occurs a massive influx of calcium into the myocardial cell to subsequently cause cardiomyopathy. This study was therefore undertaken to investigate the role of oxidative stress underlying the impaired Ca 2+ homeostasis induced by excess catecholamines during catecholamine-induced cardiomypathy. By using isoproterenol, a synthetic catecholamine, which is known to produce cardiac hypertrophy and induce biphasic changes in calcium transport, we can study the ability of cardiomyocytes in handling the intracellular calcium during oxidative stress. (Abstract shortened by UMI.)
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