| Mitochondrial energy conversion disturbance with decrease in ATP production as a source of systemic arterial hypertension. | |
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MedLine Citation:
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PMID: 17949954 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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Despite numerous efforts, including recent genetic and molecular biology studies, the immediate cause of stationary elevated blood pressure (BP) in any kind of hypertension has not been satisfactorily explained. 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 Ca(2+) 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. |
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Authors:
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Yuvenalii V Postnov; Sergei N Orlov; Yegor Y Budnikov; Alexander D Doroschuk; Anton Y Postnov |
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Publication Detail:
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Type: Journal Article Date: 2007-10-18 |
Journal Detail:
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Title: Pathophysiology : the official journal of the International Society for Pathophysiology / ISP Volume: 14 ISSN: 0928-4680 ISO Abbreviation: Pathophysiology Publication Date: 2007 Dec |
Date Detail:
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Created Date: 2007-12-06 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9433813 Medline TA: Pathophysiology Country: Netherlands |
Other Details:
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Languages: eng Pagination: 195-204 Citation Subset: - |
Affiliation:
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Russian Cardiology Research and Production Complex, Moscow, Russia. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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