ArticlePflugers Archiv : European journal of physiology2011
In vivo key role of reactive oxygen species and NHE-1 activation in determining excessive cardiac hypertrophy.
Article in Pflugers Archiv : European journal of physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 39 citations in OpenAlex.
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- The lack of slow force response in failing rat myocardium: role of stretch-induced modulation of Ca-TnC kinetics.The journal of physiological sciences : JPS · 2019Article
- Review on Chamber-Specific Differences in Right and Left Heart Reactive Oxygen Species Handling.Frontiers in physiology · 2018Article
- Cardiovascular function in male and female JCR:LA-cp rats: effect of high-fat/high-sucrose diet.American journal of physiology. Heart and circulatory physiology · 2017Article
- Exercise Attenuates Intermittent Hypoxia-Induced Cardiac Fibrosis Associated with Sodium-Hydrogen Exchanger-1 in Rats.Frontiers in physiology · 2016Article
- Transient receptor potential channels contribute to pathological structural and functional remodeling after myocardial infarction.Circulation research · 2014Article
- The autocrine/paracrine loop after myocardial stretch: mineralocorticoid receptor activation.Current cardiology reviews · 2013Review
- Roles of Na⁺/H⁺ exchanger type 1 and intracellular pH in angiotensin II-induced reactive oxygen species generation and podocyte apoptosis.Journal of pharmacological sciences · 2013Article
- The metabolic syndrome, oxidative stress, environment, and cardiovascular disease: the great exploration.Experimental diabetes research · 2012Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Growing in vitro evidence suggests NHE-1, a known target for reactive oxygen species (ROS), as a key mediator in cardiac hypertrophy (CH). Moreover, NHE-1 inhibition was shown effective in preventing CH and failure; so has been the case for AT1 receptor (AT1R) blockers. Previous experiments indicate that myocardial stretch promotes angiotensin II release and post-translational NHE-1 activation; however, in vivo data supporting this mechanism and its long-term consequences are scanty. In this work, we thought of providing in vivo evidence linking AT1R with ROS and NHE-1 activation in mediating CH. CH was induced in mice by TAC. A group of animals was treated with the AT1R blocker losartan. Cardiac contractility was assessed by echocardiography and pressure-volume loop hemodynamics. After 7 weeks, TAC increased left ventricular (LV) mass by ~45% vs. sham and deteriorated LV systolic function. CH was accompanied by activation of the redox-sensitive kinase p90(RSK) with the consequent increase in NHE-1 phosphorylation. Losartan prevented p90(RSK) and NHE-1 phosphorylation, ameliorated CH and restored cardiac function despite decreased LV wall thickness and similar LV systolic pressures and diastolic dimensions (increased LV wall stress). In conclusion, AT1R blockade prevented excessive oxidative stress, p90(RSK) and NHE-1 phosphorylation, and decreased CH independently of hemodynamic changes. In addition, cardiac performance improved despite a higher work load.
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