[Ion mechanisms of the mechanoelectrical feedback in myocardial cells].

This article is dedicated to the mechanism of mechano-electric feedback in heart. The evidence is briefly discussed on organ, tissue, cell and in details on cell membrane levels in case of application of one of applied mechanical stimulus to cardiomyocytes. Stretch of the hole heart or its tissue fragment causes quick starting repolarization of action potentials (AP)/monophasic action potentials (MAP), shift of AP/MAP plato to higher negative zone, appearance of peaks of stretch-induced depolarization (SID) on final phase of AP/MAP repolarization level, which are overgrowing into extra AP/extra MAP. Mechanical events (changes in length and force of contractions) change electrical processes by means of direct influence on cell membrane via stretch activated channels (SAC). Cardiomyocytes, isolated from animal atrium and animal and human ventricular are responsible for the stretch of depolarized membrane, prolongation of AP and appearance of extra AP (extra systoles). Analysis of experiments, conducted following the patch clamp method in whole cell configuration, shows that the main cause of that mechanical events is SAC current--ISAC. During negative potential ISAC is determined by incoming into the cell sodium ions and is negative. Negative ISAC is changing final phase of AP/MAP repolarization and causes SID, which is overgrowing into extra AP (extra systoles), in case that SID exceeds threshold. Fast AP repolarization and AP plato shift into higher negative zone is related to positive ISAC (living potassium ions through SAC), activation of IK and reduction of ISAC. Activation of ISAC and arrhythmia induction require lower mechanical stimulus for hypertrophied cardiomyocytes, in comparisment to healthy ones. Hypertrophy of cardiomyocytes can lead to expression of SAC therefore increasing channel density and ISAC maximum amplitude. In this article is discussing data, acquired by means of direct measurement of conduction of single SAC on the background of mechanical stimulation of the cardiomyocytes membrane. It contains characteristics of the estimated SACs. It is shown that blocking of conduction of ions through SAC prevents mechanically induced arrhythmia in healthy and hypertrophied cardiomyocytes, which transforms the problem of mechano-electric feedback in heart from purely fundamental into clinical one.