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Updated: Jan 25, 2026

Analysis of Cardiac Contractile Dysfunction and Ca2+ Transients in Rodent Myocytes
Published on: May 25, 2022
Ablation of B1- and B2-kinin receptors causes cardiac dysfunction through redox-nitroso unbalance
Thássio Ricardo Ribeiro Mesquita1, Rodrigo Miguel-Dos-Santos2, Itamar Couto Guedes de Jesus3
1Department of Physiology, Federal University of Sergipe, Sergipe, Brazil; Cedars-Sinai Medical Center, Smidt Heart Institute, Los Angeles, United States of America.
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.
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