Author(s): Adameova A, Abdellatif Y, Dhalla NS
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Abstract Various stressful stimuli are known to activate the sympathetic nervous system to release catecholamines and the hypothalamic-pituitary-adrenal axis to release glucocorticoids in the circulation. Although initial actions of both catecholamines and glucocorticoids are beneficial for the function of the cardiovascular system, their delayed effects on the heart are deleterious. Glucocorticoids not only increase plasma levels of catecholamines by inhibiting their extraneuronal uptake, but they have also been shown to induce supersensitivity to catecholamines in the heart by upregulating different components of the betta-adrenoceptor signal transduction system. Low concentrations of catecholamines stimulate the heart by promoting Ca2+ movements, whereas excessive amounts of catecholamines produce cardiac dysfunction by inducing intracellular Ca2+ overload in cardiomyocytes. Several studies have shown, however, that under stressful conditions high concentrations of catecholamines become oxidized to form aminolutins and generate oxyradicals. These oxidation products of catecholamines have been demonstrated to produce coronary spasm, arrhythmias, and cardiac dysfunction by inducing Ca2+-handling abnormalities in both sarcolemmal and sarcoplasmic reticulum, defects in energy production by mitochondria, and myocardial cell damage. In this article we have focused the discussion to highlight the interrelationship between catecholamines and glucocorticoids and to emphasize the role of oxidation products of catecholamines in the development of stress-induced heart disease.
This article was published in Can J Physiol Pharmacol
and referenced in Journal of Clinical & Experimental Cardiology