The transmitter depletion of the myocardium in hypertrophy and especially insufficiency has formerly been attributed to a decrease of certain enzymes that are involved in the neurotransmitter synthesis. However, we could show in human auricles recently that one main reason for the catecholamine depletion is the distension of the adrenergic ground plexus in the course of hypertrophy of the myocardial muscle cells. At the same time, electron microscope investigations revealed various changes of the axonal ultrastructure, especially in heart insufficiency. Additional experimental work in renal hypertension of rats should answer the question whether this process occurs also in other parts of the heart and whether it can be followed sequentially during the development of hypertension. In this preliminary report about these studies, attention is drawn to focal transmitter depletion in areas of severe vascular necrosis and inflammation, especially in the right ventricular wall. During the first three months after the beginning of the experiment, the total noradrenaline content decreased only slightly, whereas the concentration of this transmitter is lowered significantly by myocardial growth in both ventricles. It is concluded that there are essential differences between hypertrophy in experimental renal hypertension and human cardiac hypertrophy.