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BACKGROUND Mechanical dilation of the human ventricle is known to induce arrhythmias, the underlying ionic mechanisms, however, remain to be clarified. METHODS Ventricular myocytes isolated from human, guinea-pig or rat hearts were stretched between the patch electrode and a glass stylus. RESULTS Local stretch prolonged the action potential, depolarized(More)
OBJECTIVES Electrically non-excitable cardiac fibroblasts in the sino-atrial node region are mechano-sensitive. Rhythmic contraction of adjacent myocardium, or artificial stretch of the tissue, produce a reversible change in the membrane potential: mechanically induced potentials (MIP). Stretch of normal cardiomyocytes can be associated with intracellular(More)
The positive chronotropic response of the heart to stretch of the right atrium is one of the major mechanisms adjusting the heart rate to variations in venous return on a beat-by-beat basis. The precise pathway of this mechano-electric feedback and its cellular basis are uncertain. In this study, a possible contribution of mechanosensitive fibroblasts,(More)
Left ventricular myocardial infarction (MI) can lead to alterations in hemodynamic load conditions, thereby inducing right atrial hypertrophy and dilatation associated with phenotypic modulation of cardiomyocytes, electrical abnormalities, rhythm disturbances, and atrial fibrillation. However, there is limited information on the electrophysiological basis(More)
Electrically non-excitable but mechanosensitive right-atrial fibroblasts are thought to be involved in the chronotropic response of the heart to stretch. After myocardial infarction, altered chronotropic response may be due to the remodeling process which also involves the right atrium. Remodeling is associated with the development of hypertrophy of(More)
It has been shown that cardiac fibroblasts of the human heart are electrically non-excitable and mechanosensitive. The resting membrane potential of these cells is -15.9+/-2.1 mV and the membrane resistance is 4.1+/-0.1 G[Omega]. Rhythmic contractions of the myocardium associated with stretch of the surrounding tissue produce reversible changes in the(More)
Stretch-activated non-selective cation currents (I SAC) constitute a mechanism that can induce cardiac arrhythmias. We studied I SAC in mouse ventricular myocytes by stretching part of the cell surface between the patch-pipette and a motor-driven glass stylus. In non-clamped cells, local stretch depolarised and induced after-depolarisations and(More)
Fibroblasts in the heart can respond to mechanical deformation of the plasma membrane with characteristic changes of their membrane potential. Membrane depolarization of the fibroblasts occurs during the myocardial contractions and is caused by an influx of cations, mainly of sodium ions, into the cells. Conversely, application of mechanical stretch to the(More)
BACKGROUND Myocardial infarction can lead to electrical abnormalities and rhythm disturbances. However, there is limited data on the electrophysiological basis for these events. Since regional contraction abnormalities feature prominently in infarction, we investigated whether stretch of myocardium from the infarction borderzone can modulate the(More)
The article concentrates on representatives of voltage-gated calcium ion channels that are present in practically all cells. Regarded is the molecular arrangement of a voltage-gated calcium channel that consists of pore forming trans-membrane alpha1 subunit and auxiliary alpha2delta-, beta-, and gamma-subunits. Under discussion are the structure and(More)