Lower troponin expression in the right ventricle of rats explains interventricular differences in E-C coupling

Right ventricular cardiomyocytes show shorter action potential and smaller shortening than left cardiomyocytes. Jeon et al. suggest that interventricular differences in excitation-contraction coupling are explained by lower expression of Ca2+-binding troponin in right ventricular cardiomyocytes. Despite distinctive functional and anatomic differences, a precise understanding of the cardiac interventricular differences in excitation-contraction (E-C) coupling mechanisms is still lacking. Here, we directly compared rat right and left cardiomyocytes (RVCM and LVCM). Whole-cell patch clamp, the IonOptix system, and fura-2 fluorimetry were used to measure electrical properties (action potential and ionic currents), single-cell contractility, and cytosolic Ca2+ ([Ca2+](i)), respectively. Myofilament proteins were analyzed by immunoblotting. RVCM showed significantly shorter action potential duration (APD) and higher density of transient outward K+ current (I-to). However, the triggered [Ca2+](i) change (Ca2+ transient) was not different, while the decay rate of the Ca2+ transient was slower in RVCM. Although the relaxation speed was also slower, the sarcomere shortening amplitude (Delta SL) was smaller in RVCM. SERCA activity was similar to 60% lower in RVCM, which is partly responsible for the slower decay of the Ca2+ transient. Immunoblot analysis revealed lower expression of the cardiac troponin complex (cTn) in RVCM, implying a smaller Ca2+ buffering capacity (kappa(S)), which was proved by in situ analysis. The introduction of these new levels of cTn, I-to, and SERCA into a mathematical model of rat LVCM reproduced the similar Ca2+ transient, slower Ca2+ decay, shorter APD, and smaller Delta SL of RVCM. Taken together, these data show reduced expression of cTn proteins in the RVCM, which provides an explanation for the interventricular difference in the E-C coupling kinetics.