Difference between revisions of "Hamilton 2016 Am J Physiol Heart Circ Physiol"
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{{Publication | {{Publication | ||
|title=Hamilton DJ, Zhang A, Li S, Cao TN, Smith JA, Vedula I, Cordero-Reyes AM, Youker KA, Torre-Amione G, Gupte AA (2016) Combination of angiotensin II and l-NG-nitroarginine methyl ester exacerbates mitochondrial dysfunction and oxidative stress to cause heart failure. Am J Physiol Heart Circ Physiol 310:H667-80. ย | |title=Hamilton DJ, Zhang A, Li S, Cao TN, Smith JA, Vedula I, Cordero-Reyes AM, Youker KA, Torre-Amione G, Gupte AA (2016) Combination of angiotensin II and l-NG-nitroarginine methyl ester exacerbates mitochondrial dysfunction and oxidative stress to cause heart failure. Am J Physiol Heart Circ Physiol 310:H667-80. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/26747502 PMID: 26747502] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/26747502 PMID: 26747502] | ||
|authors=Hamilton DJ, Zhang A, Li S, Cao TN, Smith JA, Vedula I, Cordero-Reyes AM, Youker KA, Torre-Amione G, Gupte AA | |authors=Hamilton DJ, Zhang A, Li S, Cao TN, Smith JA, Vedula I, Cordero-Reyes AM, Youker KA, Torre-Amione G, Gupte AA | ||
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Copyright ยฉ 2016 the American Physiological Society. | Copyright ยฉ 2016 the American Physiological Society. | ||
|keywords=Angiotensin II, Heart failure, Mitochondria, Nitric oxide, Oxidative stress | |keywords=Angiotensin II, Heart failure, Mitochondria, Nitric oxide, Oxidative stress, Amplex Red | ||
|mipnetlab=US LA Baton Rouge Hand SC | |mipnetlab=US LA Baton Rouge Hand SC | ||
}} | }} | ||
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|diseases=Cardiovascular | |diseases=Cardiovascular | ||
|couplingstates=LEAK, OXPHOS | |couplingstates=LEAK, OXPHOS | ||
| | |pathways=F, N, S, NS, Other combinations, ROX | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|additional= | |additional=2016-03 | ||
}} | }} |
Latest revision as of 17:18, 7 November 2016
Hamilton DJ, Zhang A, Li S, Cao TN, Smith JA, Vedula I, Cordero-Reyes AM, Youker KA, Torre-Amione G, Gupte AA (2016) Combination of angiotensin II and l-NG-nitroarginine methyl ester exacerbates mitochondrial dysfunction and oxidative stress to cause heart failure. Am J Physiol Heart Circ Physiol 310:H667-80. |
Hamilton DJ, Zhang A, Li S, Cao TN, Smith JA, Vedula I, Cordero-Reyes AM, Youker KA, Torre-Amione G, Gupte AA (2016) Am J Physiol Heart Circ Physiol
Abstract: Mitochondrial dysfunction has been implicated as a cause of energy deprivation in heart failure (HF). Herein, we tested individual and combined effects of two pathogenic factors of nonischemic HF, inhibition of nitric oxide synthesis [with l-N(G)-nitroarginine methyl ester (l-NAME)] and hypertension [with angiotensin II (AngII)], on myocardial mitochondrial function, oxidative stress, and metabolic gene expression. l-NAME and AngII were administered individually and in combination to mice for 5 wk. Although all treatments increased blood pressure and reduced cardiac contractile function, the l-NAME + AngII group was associated with the most severe HF, as characterized by edema, hypertrophy, oxidative stress, increased expression of Nppa and Nppb, and decreased expression of Atp2a2 and Camk2b. l-NAME + AngII-treated mice exhibited robust deterioration of cardiac mitochondrial function, as observed by reduced respiratory control ratios in subsarcolemmal mitochondria and reduced state 3 levels in interfibrillar mitochondria for complex I but not for complex II substrates. Cardiac myofibrils showed reduced ADP-supported and oligomycin-inhibited oxygen consumption. Mitochondrial functional impairment was accompanied by reduced mitochondrial DNA content and activities of pyruvate dehydrogenase and complex I but increased H2O2 production and tissue protein carbonyls in hearts from AngII and l-NAME + AngII groups. Microarray analyses revealed the majority of the gene changes attributed to the l-NAME + AngII group. Pathway analyses indicated significant changes in metabolic pathways, such as oxidative phosphorylation, mitochondrial function, cardiac hypertrophy, and fatty acid metabolism in l-NAME + AngII hearts. We conclude that l-NAME + AngII is associated with impaired mitochondrial respiratory function and increased oxidative stress compared with either l-NAME or AngII alone, resulting in nonischemic HF.
Copyright ยฉ 2016 the American Physiological Society. โข Keywords: Angiotensin II, Heart failure, Mitochondria, Nitric oxide, Oxidative stress, Amplex Red
โข O2k-Network Lab: US LA Baton Rouge Hand SC
Labels: MiParea: Respiration, mt-Medicine
Pathology: Cardiovascular
Stress:Oxidative stress;RONS
Organism: Mouse
Tissue;cell: Heart
Preparation: Permeabilized tissue, Isolated mitochondria
Coupling state: LEAK, OXPHOS
Pathway: F, N, S, NS, Other combinations, ROX
HRR: Oxygraph-2k
2016-03