To the development of the membrane conception of primary hypertension (altered mitochondrial function and energy deficiency)

The author proceeds from the idea that the phenomenon of increased arterial blood pressure (BP), which reflects the shift of the set-point in the BP c ontrolling system, is conditioned by an underlying energy deficiency at the cellular level. The paths leading to this deficiency, its causes and its d istribution in the tissues are different for each specific form of hyperten sion, but the underlying pathogenetic mechanism is apparently realized via a decrease of the energy generating function of mitochondria. As an example of energydependence of the hypertension phenomenon one may consider system ic blood pressure elevation in hyperthyroidism las a result of oxidation-ph osphorylation uncoupling, which leads to decreased ATP production by the mi tochondria). In primary hypertension (essential hypertension of men and spo ntaneous hypertension of rats, SHR) one can speak of the existence of genet ically determined traits of cell membranes (the so-called membrane defect) leading to insufficient control over intracellular calcium and to the appea rance of increased concentrations of cytosolic free calcium under the physi ological action on mechanisms of cell calcium homeostasis. Mediated by augm ented efferent sympathetic activity, the sustained elevation of BP occurs a s far as the excess of cytosolic calcium accumulates in mitochondria and th eir energy generating function decreases, resulting in subsequent alteratio ns in the ion transport Function of cell membranes. Thus, increased systemi c blood pressure in the case of primary hypertension should be regarded as an inherent feature of blood circulation corresponding to a lowered level o f cell energetics. The specific features distinguishing essential hypertens ion from other inherited diseases and the wider outlook on its pathogenesis clarify the essence of the genomic process that determines its development . The experimental model of primary hypertension (SHR) confirms the assumpt ion that the physical basis of the latter is the rearrangement of clusters of moderate repeats of genomic DNA.