Institute of Immunology and Physiology, Russian Academy of Sciences, Pervomajskaya 106, 620049, Yekaterinburg, Russia.
Institute of Immunology and Physiology, Russian Academy of Sciences, Pervomajskaya 106, 620049, Yekaterinburg, Russia.
Biochem Biophys Res Commun. 2021 Feb 19;541:30-35. doi: 10.1016/j.bbrc.2020.12.102. Epub 2021 Jan 15.
Estrogen deficiency has a significant influence on the excitation-contraction coupling in the ventricular myocardium but its impact on the atrial contractile function has not been studied. We have compared the effects of estrogen deficiency on the contractility and cytosolic Ca transient of single cardiomyocytes isolated from the left atrium (LA) and the left ventricle (LV) of rats subjected to ovariectomy (OVX) or sham surgery (Sham). The characteristics of actin-myosin interaction were studied in an in vitro motility assay. We found that OVX decreased the contractility of LV single cardiomyocytes but increased that of LA myocytes. The disturbance of ventricular mechanical function may be explained by the acceleration of Ca transient and reduced Ca sensitivity of the actin-myosin interaction. The augmentation of LA contractility may be explained by accelerated cross-bridge kinetics and increased end-diastolic sarcomere length, which may lead to elevated tension in atrial cells due to the Frank-Starling mechanism.
雌激素缺乏对心室心肌的兴奋-收缩偶联有显著影响,但对心房收缩功能的影响尚未研究。我们比较了雌激素缺乏对去卵巢(OVX)或假手术(Sham)大鼠左心房(LA)和左心室(LV)分离的单个心肌细胞收缩性和细胞浆钙瞬变的影响。在体外运动分析中研究了肌动球蛋白相互作用的特征。我们发现,OVX 降低了 LV 单个心肌细胞的收缩性,但增加了 LA 心肌细胞的收缩性。心室机械功能的紊乱可以通过钙瞬变的加速和肌动球蛋白相互作用的钙敏感性降低来解释。LA 收缩性的增强可以通过加快横桥动力学和增加舒张末期肌节长度来解释,这可能由于 Frank-Starling 机制导致心房细胞张力升高。