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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Role of the excessive amounts of circulating catecholamines and glucocorticoids in stress-induced heart disease.
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Role of the excessive amounts of circulating catecholamines and glucocorticoids in stress-induced heart disease.

机译:过量的循环儿茶酚胺和糖皮质激素在应激性心脏病中的作用。

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摘要

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.
机译:已知各种压力刺激可激活交感神经系统以释放儿茶酚胺,而下丘脑-垂体-肾上腺轴释放循环中的糖皮质激素。尽管儿茶酚胺和糖皮质激素的初始作用都有益于心血管系统的功能,但它们对心脏的延迟作用是有害的。糖皮质激素不仅通过抑制它们的神经外摄取而增加儿茶酚胺的血浆水平,而且还显示出它们通过上调betta-肾上腺素受体信号转导系统的不同成分来诱导心脏对儿茶酚胺的超敏性。低浓度的儿茶酚胺通过促进Ca2 +运动来刺激心脏,而过量的儿茶酚胺则通过诱导心肌细胞的细胞内Ca2 +超负荷而产生心脏功能障碍。但是,一些研究表明,在压力条件下,高浓度的儿茶酚胺会被氧化形成氨基黄嘌呤并生成羟自由基。已经证明,儿茶酚胺的这些氧化产物通过诱导肌膜和肌浆网中的Ca2 +处理异常,线粒体产生的能量产生缺陷以及心肌细胞损伤,从而产生冠状动脉痉挛,心律不齐和心脏功能障碍。在本文中,我们集中讨论以突出儿茶酚胺和糖皮质激素之间的相互关系,并强调儿茶酚胺的氧化产物在应激性心脏病发展中的作用。

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