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DOI 10.1016/j.lfs.2019.04.062

Медицинская библиотека · Life sciences · 2019

Ablation of B1- and B2-kinin receptors causes cardiac dysfunction through redox-nitroso unbalance.

Mesquita Thássio Ricardo Ribeiro, Miguel-Dos-Santos Rodrigo, Jesus Itamar Couto Guedes de, de Almeida Grace Kelly Melo, Fernandes Valéria Alves, Gomes Aline Alves Lara, Guatimosim Silvia, Martins-Silva Leonardo, Ferreira Anderson José, Capettini Luciano Dos Santos Aggum, Pesquero Jorge Luís, Lauton-Santos Sandra

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Аннотация

AIMS: B1- and B2-kinin receptors play a major role in several cardiovascular diseases. Therefore, we aimed to evaluate cardiac functional consequences of B1- and B2-kinin receptors ablation, focusing on the cardiac ROS and NO generation.

MAIN

METHODS

Cardiac contractility, ROS, and NO generation, and protein expression were evaluated in male wild-type (WT), B1- (B1-/-) and B2-kinin (B2-/-) knockout mice.

KEY FINDINGS: Impaired contractility in B1-/- and B2-/- hearts was associated with oxidative stress through upregulation of NADPH oxidase p22phox subunit. B1-/- and B2-/- hearts presented higher NO and peroxynitrite levels than WT. Despite decreased sarcoplasmic reticulum Ca2+ ATPase pump (SERCA2) expression, nitration at tyrosine residues of SERCA2 was markedly higher in B1-/- and B2-/- hearts.

SIGNIFICANCE: B1- and B2-kinin receptors govern ROS generation, while disruption of B1- and B2-kinin receptors leads to impaired cardiac dysfunction through excessive tyrosine nitration on the SERCA2 structure.

Для цитирования: Mesquita Thássio Ricardo Ribeiro, Miguel-Dos-Santos Rodrigo, Jesus Itamar Couto Guedes de, de Almeida Grace Kelly Melo, Fernandes Valéria Alves, Gomes Aline Alves Lara, Guatimosim Silvia, Martins-Silva Leonardo, Ferreira Anderson José, Capettini Luciano Dos Santos Aggum, Pesquero Jorge Luís, Lauton-Santos Sandra. Ablation of B1- and B2-kinin receptors causes cardiac dysfunction through redox-nitroso unbalance.. Life sciences. 2019. DOI: 10.1016/j.lfs.2019.04.062.

Предметные рубрики MeSH

AnimalsGene DeletionHeartHeart DiseasesMaleMiceMice, Inbred C57BLMice, KnockoutMyocardial ContractionNADPH OxidasesNitric OxideOxidation-ReductionReactive Oxygen SpeciesReceptor, Bradykinin B1Receptor, Bradykinin B2
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