Ablation of B1- and B2-kinin receptors causes cardiac dysfunction through redox-nitroso unbalance.
Life Sci
; 228: 121-127, 2019 Jul 01.
Article
en En
| MEDLINE
| ID: mdl-31039364
ABSTRACT
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. MAINMETHODS:
Cardiac contractility, ROS, and NO generation, and protein expression were evaluated in male wild-type (WT), B1- (B1-/-) and B2-kinin (B2-/-) knockout mice. KEYFINDINGS:
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.Palabras clave
Texto completo:
1
Base de datos:
MEDLINE
Asunto principal:
Receptor de Bradiquinina B1
/
Receptor de Bradiquinina B2
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Corazón
/
Cardiopatías
Tipo de estudio:
Etiology_studies
Límite:
Animals
Idioma:
En
Revista:
Life Sci
Año:
2019
Tipo del documento:
Article