title: [Mitochondrial energy conversion disturbance with decrease in ATP production as a source of systemic arterial hypertension].
abstract: This review deals with the cellular mechanisms underlying decreased energy status documented in different tissues from experimental rat models of primary and secondary hypertension as well as the involvement of these abnormalities in the pathogenesis of the disease. Such analyses allow us to hypothesize that dysfunction of mitochondrial energy conversion, caused by distinct stimuli, including generalized disturbances of intracellular Ca2+ handling and mitochondria calcium overload found in primary hypertension, leads to uncoupling of oxidation and phosphorylation and attenuated ATP synthesis. Examples of arterial hypertension accompanied by mitochondrial uncoupling and cell ATP depletion (hyperthyroidism, cold hypertension, cyclosporine A intake, etc.) may be considered as an additional argument supporting this opinion. It means also that despite of differences in triggering mechanisms of mitochondrial dysfunction in all these models, the final outcome, i.e. decreased mitochondrial ATP production, is similar. Attenuated intracellular ATP content, in turn, results in the long-term maintenance of elevated BP by increased sympathetic outflow, whereas augmented ROS production following mitochondrial dysfunction lowers the capacity of the NO-dependent vascular relaxation. In the light of these data the cause of stationary elevated BP in chronic arterial hypertension should be regarded as a compensatory response to decreased mitochondrial ATP synthesis.
authors.forename: Iu V
authors.initials: IuV
authors.lastname: Postnov
authors.forename: S N
authors.initials: SN
authors.lastname: Orlov
authors.forename: E Iu
authors.initials: EIu
authors.lastname: Budnikov
authors.forename: A D
authors.initials: AD
authors.lastname: Doroshchuk
authors.forename: A Iu
authors.initials: AIu
authors.lastname: Postnov
mesh_terms: D000255:Adenosine Triphosphate / Q000502:physiology*; D000818:Animals; D015220:Calcium Channels / Q000378:metabolism; D004734:Energy Metabolism / Q000502:physiology*; D006973:Hypertension / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology*; D008929:Mitochondria, Heart / Q000378:metabolism / Q000473:pathology / Q000502:physiology*; D025261:Mitochondrial Proton-Translocating ATPases / Q000378:metabolism; D051381:Rats; D017382:Reactive Oxygen Species
chemical_list: D015220:Calcium Channels; D017382:Reactive Oxygen Species; D000255:Adenosine Triphosphate; D025261:Mitochondrial Proton-Translocating ATPases