Literature DB >> 19330604

Reactive oxygen species and dopamine receptor function in essential hypertension.

Chunyu Zeng1, Van Anthony M Villar, Peiying Yu, Lin Zhou, Pedro A Jose.   

Abstract

Essential hypertension is a major risk factor for stroke, myocardial infarction, and heart and kidney failure. Dopamine plays an important role in the pathogenesis of hypertension by regulating epithelial sodium transport and by interacting with vasoactive hormones and humoral factors. However, the mechanisms leading to impaired dopamine receptor function in hypertension states are not clear. Compelling experimental evidence indicates a role of reactive oxygen species (ROS) in hypertension, and there are increasing pieces of evidence showing that in conditions associated with oxidative stress, which is present in hypertensive states, dopamine receptor effects, such as natriuresis, diuresis, and vasodilation, are impaired. The goal of this review is to present experimental evidence that has led to the conclusion that decreased dopamine receptor function increases ROS activity and vice versa. Decreased dopamine receptor function and increased ROS production, working in concert or independent of each other, contribute to the pathogenesis of essential hypertension.

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Year:  2009        PMID: 19330604      PMCID: PMC3722595          DOI: 10.1080/10641960802621283

Source DB:  PubMed          Journal:  Clin Exp Hypertens        ISSN: 1064-1963            Impact factor:   1.749


  170 in total

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4.  Lipoic acid prevents hypertension, hyperglycemia, and the increase in heart mitochondrial superoxide production.

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5.  Concordance of murine quantitative trait loci for salt-induced hypertension with rat and human loci.

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Authors:  Pietro Minuz; Paola Patrignani; Stefania Gaino; Francesca Seta; Marta L Capone; Stefania Tacconelli; Maurizio Degan; Giovanni Faccini; Anna Fornasiero; Giorgio Talamini; Rosamaria Tommasoli; Enrico Arosio; Clara Lechi Santonastaso; Alessandro Lechi; Carlo Patrono
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9.  Intrarenal dopamine attenuates deoxycorticosterone acetate/high salt-induced blood pressure elevation in part through activation of a medullary cyclooxygenase 2 pathway.

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