Differing effects of estrogen deficiency on the contractile function of atrial and ventricular myocardium

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 2+ 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 2+ transient and reduced Ca 2+ 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. • Ovariectomy (OVX) has opposite effects on LA and LV contractility. • OVX affects differently the actin-myosin interaction in LA and LV. • OVX changes differently the Ca 2+ transient in LA and LV. • OVX changes sarcomere protein phosphorylation in LA and LV in different ways. • The observed differences can lead to heart failure.