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

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. Cardiac contractility, ROS, and NO generation, and protein expressio...

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Bibliographic Details
Published in:Life sciences (1973) 2019-07, Vol.228, p.121-127
Main Authors: 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
Format: Article
Language:English
Subjects:
Ablation
Adenosine triphosphatase
Ca2+-transporting ATPase
Calcium (reticular)
Calcium ions
Cardiac
Cardiac muscle
Cardiovascular diseases
Heart diseases
Kinin receptors
Muscle contraction
NAD(P)H oxidase
NADPH oxidase
Nitration
Nitric oxide
Oxidative stress
Peroxynitrite
Reactive oxygen species
Receptors
Sarcoplasmic reticulum
Tyrosine
Unbalance
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Summary: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. Cardiac contractility, ROS, and NO generation, and protein expression were evaluated in male wild-type (WT), B1- (B1−/−) and B2-kinin (B2−/−) knockout mice. 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. 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.
ISSN:0024-3205
1879-0631
DOI:10.1016/j.lfs.2019.04.062