| The Na+/Ca2+ exchanger-1 mediates left ventricular dysfunction in mice with chronic intermittent hypoxia. | |
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MedLine Citation:
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PMID: 20947716 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Chronic intermittent hypoxia (CIH) and cardiovascular dysfunction occur in patients with obstructive sleep apnea. We hypothesized that the Na(+)/Ca(2+) exchanger-1 (NCX1) mediates, at least partially, left ventricular (LV) dysfunction in CIH. Four groups of mice (N = 15-17 per group), either cardiac-specific NCX1 knockouts (KO) or wild types (WT), were exposed to either CIH or normoxia [i.e., handled controls (HC)] 10 h/day for 8 wk. As expected, myocardial expression of NCX1 was greater in WT than in KO animals, both in HC and CIH-exposed groups. In both CIH groups (WT or KO), but not the HC groups, blood pressure increased by 10% at week 1 over their baseline and remained elevated for all 8 wk, with no differences between WT and KO. LV dilation (increased diastolic and systolic dimension) and hypertrophy (increased left heart weight), along with LV dysfunction (greater end-diastolic pressure and lower ejection fraction), were observed in the WT animals compared with the KO following CIH exposure. Compared with HC, CIH exposure was associated with apoptosis (terminal deoxynucleotidyl transferase dUTP-mediated nick-end labeling and caspase-3) in WT, but not KO, mice. We conclude that myocardial NCX1 does not mediate changes in blood pressure, but is one of the mediators for LV global dysfunction and cardiomyocyte injury in CIH. |
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Authors:
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Ling Chen; Jin Zhang; Xuejiao Hu; Kenneth D Philipson; Steven M Scharf |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2010-10-14 |
Journal Detail:
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Title: Journal of applied physiology (Bethesda, Md. : 1985) Volume: 109 ISSN: 1522-1601 ISO Abbreviation: J. Appl. Physiol. Publication Date: 2010 Dec |
Date Detail:
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Created Date: 2010-12-14 Completed Date: 2011-03-25 Revised Date: 2011-12-21 |
Medline Journal Info:
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Nlm Unique ID: 8502536 Medline TA: J Appl Physiol Country: United States |
Other Details:
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Languages: eng Pagination: 1675-85 Citation Subset: IM |
Affiliation:
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Department of Medicine, University of Maryland, Baltimore, Maryland, USA. Lchen@medicine.umaryland.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Anoxia / complications, diagnosis, metabolism*, pathology, physiopathology Apoptosis Blood Pressure Body Weight Cardiomegaly / etiology, metabolism Caspase 3 / metabolism Chronic Disease Disease Models, Animal Echocardiography Gene Expression Regulation Heart Catheterization Male Mice Mice, Inbred C57BL Mice, Knockout Myocardium / metabolism* RNA, Messenger / metabolism Sodium-Calcium Exchanger / genetics, metabolism* Stroke Volume Time Factors Ventricular Dysfunction, Left / diagnosis, etiology, metabolism*, pathology, physiopathology Ventricular Function, Left* |
| Grant Support | |
ID/Acronym/Agency:
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HL074441/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/NCX1 protein, mouse; 0/RNA, Messenger; 0/Sodium-Calcium Exchanger; EC 3.4.22.-/Casp3 protein, mouse; EC 3.4.22.-/Caspase 3 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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