容量过载诱导心肌肥厚时大鼠心脏β -肾上腺素能受体和脂肪细胞的变化。

G Cartagena, M Sapag-Hagar, J Jalil, V Tapia, E Guarda, R Foncea, R Corbalan, R Ebensperger, S Lavandero
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引用次数: 0

摘要

交感神经系统的刺激引起的心脏β -肾上腺素能受体(β - ar)的改变是导致心脏肥厚和心力衰竭的重要因素之一。在这项研究中,我们提出利用脂肪细胞替代主要含有β 2-AR亚型的循环淋巴细胞,以方便地评估实验性,容量过载诱导的大鼠心脏肥厚的心力衰竭。利用该模型,我们测量了雄性大鼠在主动脉-腔瘘形成后2、7、21和56天的心脏和脂肪细胞中的β - ar。然而,心脏β - ar密度从第7天到第21天增加(58%),随后在第56天减少(30%)[变化以对照组的百分比表示;在研究的任何时间间隔内均未记录到β - ar亲和力(Kd)的显著变化],脂肪细胞β - ar密度从第21天开始逐渐增加(87%),并持续到研究期结束(131%)。两种组织中β - ar群体缺乏相关性,因此需要对心脏和脂肪细胞中的β - 1-AR亚型进行特异性评估,以评估脂肪细胞作为评估心力衰竭的替代方法的有效性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Changes in beta-adrenergic receptors of rat heart and adipocytes during volume-overload induced cardiac hypertrophy.

Modification of cardiac beta-adrenergic receptors (beta-AR), resulting from the stimulation of the sympathetic nervous system, is one of the most important factors in the generation of cardiac hypertrophy and heart failure. In this research, we propose the utilization of adipocytes as an alternative to the use of predominantly beta 2-AR subtype containing circulating lymphocytes for the convenient assessment of cardiac failure in the experimentally, volume-overload induced heart hypertrophy in rats. Using this model, we measured beta-AR both in the heart and adipocytes of male rats 2, 7, 21 and 56 days after creating an aorta-cava fistula. Whereas an increase (58%) in cardiac beta-AR density from day 7 to 21 was followed by a decrease in this measurement (30%) on day 56 [changes expressed as percentage of controls; no significant changes in beta-AR affinity (Kd) were recorded at any of the time interval studied], adipocytes beta-AR density showed a progressive increase starting on day 21 (87%) which continued until the end (131%) of the study period. This lack of correlation of the beta-AR population in both tissues supports the need for a specific evaluation of the beta 1-AR subtype in the heart and adipocyte in order to evaluate the usefulness of adipocyte cells as an alternative to assess cardiac failure.

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