Changes in zinc metabolism and its redistribution within intracellular compartments
appear in the course of arterial hypertension. These changes may result in zinc deficiency,
which in turn may impair myocardial compensatory and reconstructive processes, increase
left ventricular load, and eventually lead to left ventricular failure. There is experimental
evidence of the role of zinc in blood pressure regulation and zinc deficiency in the course of
arterial hypertension, and there is an ongoing discussion on the role of zinc supplemen-tation in various pathological states of the organism [4, 5]. The relationship between zinc
metabolism and heart muscle hypertrophy has not been yet established