[Action of La3+ on the systems providing contractility of vertebrate myocardium]

The inotropic action of La3+ on frog myocardium was studied with taking into account of its effect on mitochondria of cardiomyocytes (CM). It has been established that in the range of studied concentrations (0.2-6 mM), La3+ decreases dose-dependently the strength of cardiac contractions (by 3.3-92.2 %). In parallel experiments on isolated rat heart mitochondria (RHM), La3+ at a concentration of 25 microM has been shown to cause swelling of non-energized and energized mitochondria in isotonic medium with 125 mM NH4NO3 and in hypotonic medium with 25 mM CH3COOK. The study of oxidative processes in mitochondria with aid of polarographic method of measurement of oxygen concentration has shown that La3+ at concentrations of 50 and 100 microM increases the oxygen consumption rate by mitochondria in the state 2. However, La3+ does not decrease the respiration rate of isolated mitochondria in the state 3, as this takes place in the case of use of Cd2+ or at the Ca(2+)-overloading of mitochondria. The rate of endogenous respiration of isolated mitochondria in the medium with La3+ was higher than in control, which implies its effect on ion permeability of the inner membrane. The data obtained in this work indicate that the La(3+)-produced decrease of the contractility of cardiac muscle is not only due to the direct blocking effect on the potential-controlled Ca2+ channels, but is also mediated by its unspecific action on the CM mitochondria. This action is manifested in acceleration of the energy-dependent K+ transport in matrix and in an increase of ion permeability of the inner mitochondrial membrane (IMM).