Abstract <p>Heterometric regulation of myocardial contractility is themost important property regulating the pumping function of the heart.Calcium ions play a key role in the activation and regulation ofmuscle contraction. In addition to changes in the degree of actin-myosinfilament overlap, one consequence of myocardial stretch is a length-dependentchange in the shape and duration of the intracellular calcium transient(CaT). As the degree of myocardial stretch increases, the durationof the CaT decreases in the upper half of the CaT decline and increasesin the lower half. To determine the contribution of myosin cross-bridgekinetics to CaT changes, length-dependent changes in CaT were assessedin three states of myosin cross-bridge kinetics; (1) intact, (2)slowed under the influence of omecamtiv mecarbil 1 µM (OM), and(3) blocked under the influence of blebbistatin 10 µM (BB). It wasfound that length-dependent multidirectional changes in CaT decay(CaT crossover phenomenon) were pronounced in the right ventricular(RV) myocardium and weak in the right atrial (RA) myocardium ofintact male nine-week-old Wistar rats. OM significantly slows therate of tension development and decline in myocardium of RA andRV rats; enhances length-dependent changes in CaT duration; OM decreasesthe duration of CaT at 80% of its amplitude and increases the durationof CaT at 20% of its amplitude in both RA and RV. BB almost completelyabolishes the ability of the myocardium to develop tension; length-dependent changesin CaT duration are monotonous, CaT crossover in RV myocardium disappears.The phenomenon of CaT crossover in the myocardium of the RV is aconsequence of the attachment and detachment of myosin cross-bridgesto the thin filament. The absence of length-dependent changes in CaTin rat RA myocardium seems to be associated with a more developedcalcium sequestering system in RA, in comparison with the calciumsequestering system in RV.</p>