[Insufficient ATP production due to mitochondrial calcium overload as a source of blood pressure elevation in primary hypertension].
The author develops previously expressed hypothesis of causative relationship between primary hypertension and altered mitochondrial energy production, reduced ATP synthesis and tissue energy deficit. These deviations in energy metabolism originate on the basis of generalized alteration of membrane regulation of intracellular Ca(2+) distribution leading to mitochondrial calcium overload and lowering of ATP synthesis. Critical factor determining mitochondrial calcium overload is the development of functional insufficiency of mPT pores of inner mitochondrial membrane facilitate Ca(2+) outflow from matrix of organelles. Elevation of systemic blood pressure is associated with emergence of energy deficit in brain tissue which stimulate vasomotor centers of brain stem and efferent activity of sympathetic nervous system supplying cardiovascular system. Stationary elevated blood pressure level in long term is supported by structural-functional rearrangement of circulation. Important component of the latter is reduction of capillary net and related centralization of circulation. Blood pressure in the central part of the arterial system is determined by demands of new level of energy metabolism in cells.
Postnov
Iu V
IuV
D000255:Adenosine Triphosphate / Q000172:deficiency*; D002118:Calcium / Q000378:metabolism*; D006801:Humans; D006973:Hypertension / Q000378:metabolism* / Q000503:physiopathology*; D008929:Mitochondria, Heart / Q000378:metabolism*
D000255:Adenosine Triphosphate; D002118:Calcium