The role of mitochondrial calcium overload and energy deficiency in pathogenesis of arterial hypertension]

The author proceeds that increased arterial blood (BP) pressure, reflecting the shift of the threshold blood pressure controlling system, is conditioned by underlying energy deficiency at the cellular level, caused by a decrease of the mitochondrial energy generating function. Elevation of systemic BP in hyperthyroidism resultant from oxidation-phosphorylation uncoupling, leading to decrease of ATP production by mitochondria, is an example of energy dependence of the hypertension phenomenon. In primary hypertension (essential hypertension in humans and spontaneous hypertension in rats) one can speak about genetically determined characteristics of cell membranes (so-called membrane defect) leading to insufficient regulation of intracellular calcium and increased concentrations of free calcium in the cytosol under physiological actions on cell calcium homeostasis mechanisms. Elevation of BP mediated by increased efferent sympathetic activity occurs as far as the excess of the cytosolic calcium accumulates in the mitochondria and their energy generating function decreases, which results in alteration of the ion transporting function of cell membranes. Hence, increased systemic BP in primary hypertension should be considered as an inherent feature of circulation corresponding to altered cell energetics.