Inter‐ventricular difference in the excitation‐contraction coupling and myofilament proteins of rat cardiomyocytes

Abstract

The left (LV) and right ventricle (RV) have distinctive structural and functional characteristics; thinner free wall and different kinetics of contraction‐relaxation in RV. However, the precise comparison of the excitation‐contraction (E‐C) coupling mechanisms and the Ca2+ homeostasis in the isolated cardiomyocytes are lacking, especially in rats. Whole‐cell patch clamp study showed significantly shorter action potential duration (APD) in RV myocytes. Consistently, the amplitude of transient outward K+ current (Ito) was higher in RV, whereas the amplitude of L‐type Ca2+ current was not different. However, when measuring the [Ca2+]i and sarcomere length (SL) of intact myocytes by using IonOptics, the Ca2+ transient amplitudes and shapes were not significantly different. Nevertheless, the accompanied shortening of SL was smaller and the speed of relaxation appeared slower in RV than LV myocytes. Interestingly, the immunoblot analysis revealed lower expression of cardiac troponin complex proteins (cTnC, cTnI, cTnT) and nebulette in RV myocytes. The lower level of Ca2+‐binding cTnC, i.e. smaller Ca2+‐buffering capacity, might be responsible for, at least partly, the similar Ca2+ transient despite the shorter APD in RV myocytes. Introduction of the higher Ito and lower cTn into the mathematical computer simulation of rat ventricular myocytes showed changes similar with the experimental data of Ca2+ transient and of contraction from the RV myocytes. Taken together, in addition to the comprehensive physiological analysis, we firstly show the lower expression of cTn proteins in the RV myocytes, which gives a clue to explain the inter‐ventricular difference in the E‐C coupling kinetics.