Introduction
In the heart gap junction intercellular coupling represents the fundament of proper electrical propagation. In cardiac hypertrophy up-regulation of Cx43 has been observed and was suggested as being related to sudden cardiac death. It has been found, that expression and distribution of Cx43, which is the main gap junction forming connexin in the ventricle, is altered in many pathological conditions. We therefore wanted to elucidate whether exposure of cardiomyocytes to chronic pulsatile stretch affects Cx43 and whether mechanotransduction pathways interfere with adrenergic regulation of Cx43, already shown in former experiments.