title: [Energy-dependent pathogenesis in chronic hypertension].
abstract: The review compiled mainly from the works of the author's laboratory continues to develop a new area in arterial hypertension studies. The author considers the major manifestation of the pathology, i. e. the stable increase in systemic blood pressure (BP), is in a direct causal relationship to cell and tissue energy deficiency. The energy deficiency is caused by impaired energy conversion in the cell mitochondria, uncoupling of oxidation and phosphorylation, and decreased ATP production. The cause of the latter in primary hypertension may be a mitochondrial calcium overload resulting from generalized abnormalities in membranous cytosol Ca2+ concentration regulation. In secondary forms of hypertension, uncoupling agents, such as thyroid hormones, angiotensin II, cyclosporine II, low temperatures, etc., may act as triggers of mitochondrial dysfunction. Hypertension begins with the activation of an efferent component of the sympathetic nervous system that supplies the vascular periphery. The sympathetic centers in the medulla oblongata seem to be involved in the activation process. Elevated systemic BP develops in order to compensate for ATF deficiency as a measure for correcting metabolic disturbances. Further systemic BP stabilization occurs with the involvement of the kidney that, exposed to elevated BP, begins functioning in a special switching (shifting) mode. Such a mode allows the kidney to avoid salt and water losses and at the same time to maintain the required (elevated) systemic BP, by affecting the mechanism of intrarenal regulation on the feedback principle. Resetting fixation takes place with the development of sclerotic changes in the kidney and hyalinosis in the renal medulla. Vascular system remodeling, including myocardial hypertrophic changes and capillary network rarefaction, is an essential element of BP stabilization. Hypertension becomes irreversible, by losing the features of compensatory and adaptive nature, and refractory to antihypertensive therapy.
authors.forename: Iu V
authors.initials: IuV
authors.lastname: Postnov
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism*; D001794:Blood Pressure / Q000502:physiology; D002118:Calcium / Q000378:metabolism; D002908:Chronic Disease; D004734:Energy Metabolism; D006801:Humans; D006973:Hypertension / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D008928:Mitochondria / Q000502:physiology*
chemical_list: D000255:Adenosine Triphosphate; D002118:Calcium