Expression and function of atrial myosin light chain 1 in the porcine right ventricle of normal and pulmonary hypertensive animals.

We investigated the expression of atrial myosin light chain 1 (ALC-1) and myosin cycling kinetics in the normal and hypertrophied right ventricle of the neonatal porcine heart. Right ventricular hypertrophy was induced by exposing piglets immediately after birth to hypobaric hypoxia for 3 days. Control piglets were kept under normal conditions for the same time. ALC-1 expression in the hypertrophied right ventricle was 16.9%. No ALC-1 expression could be observed in the right ventricle of control pigs. Force-velocity of chemically skinned right ventricular fibers was analyzed in order to examine the functional role of ALC-1 expression on myosin cross-bridge kinetics. Force generation per cross-section at maximal Ca2+ activation (pCa 4.5) was significantly higher in the hypertrophied group. Maximal shortening velocity (Vmax) of skinned fibers increased statistically significant from 0.69 muscle length per second (ML/s) in the control to 1.2 ML/s in the hypertrophied right ventricle. We conclude that the expression of ALC-1 in the hypertrophied ventricle of neonatal pigs increased cross-bridge cycling kinetics and contractility.