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Roles and Mechanisms of Dopamine Receptor Signaling in Catecholamine Excess Induced Endothelial Dysfunctions.
Yang, Zhen; Li, Yingrui; Huang, Mengying; Li, Xin; Fan, Xuehui; Yan, Chen; Meng, Zenghui; Liao, Bin; Hamdani, Nazha; Yang, Xiaoli; Zhou, Xiaobo; El-Battrawy, Ibrahim; Akin, Ibrahim.
Afiliación
  • Yang Z; Department of Ophthalmology, Affiliated Hospital of North Sichuan Medical College, 637000 Nanchong, Sichuan, China.
  • Li Y; First Department of Medicine, Medical Faculty Mannheim, University Medical Centre Mannheim (UMM), Heidelberg University, 68167 Mannheim, Germany.
  • Huang M; First Department of Medicine, Medical Faculty Mannheim, University Medical Centre Mannheim (UMM), Heidelberg University, 68167 Mannheim, Germany.
  • Li X; First Department of Medicine, Medical Faculty Mannheim, University Medical Centre Mannheim (UMM), Heidelberg University, 68167 Mannheim, Germany.
  • Fan X; First Department of Medicine, Medical Faculty Mannheim, University Medical Centre Mannheim (UMM), Heidelberg University, 68167 Mannheim, Germany.
  • Yan C; First Department of Medicine, Medical Faculty Mannheim, University Medical Centre Mannheim (UMM), Heidelberg University, 68167 Mannheim, Germany.
  • Meng Z; Key Laboratory of Medical Electrophysiology of Ministry of Education and Medical Electrophysiological Key Laboratory of Sichuan Province, Institute of Cardiovascular Research, Southwest Medical University, 646000 Sichuan, China.
  • Liao B; First Department of Medicine, Medical Faculty Mannheim, University Medical Centre Mannheim (UMM), Heidelberg University, 68167 Mannheim, Germany.
  • Hamdani N; First Department of Medicine, Medical Faculty Mannheim, University Medical Centre Mannheim (UMM), Heidelberg University, 68167 Mannheim, Germany.
  • Yang X; Department of Cardiac Macrovascular Surgery, Affiliated Hospital of Southwest Medical University, 646000 Sichuan, China.
  • Zhou X; Department of Cellular and Translational Physiology, Institute of Physiology, Ruhr University Bochum, 44801 Bochum, Germany and Institut für Forschung und Lehre (IFL), Molecular and Experimental Cardiology, Ruhr University Bochum, 44801 Bochum, Germany.
  • El-Battrawy I; Department of Ophthalmology, Affiliated Hospital of North Sichuan Medical College, 637000 Nanchong, Sichuan, China.
  • Akin I; First Department of Medicine, Medical Faculty Mannheim, University Medical Centre Mannheim (UMM), Heidelberg University, 68167 Mannheim, Germany.
Int J Med Sci ; 21(10): 1964-1975, 2024.
Article en En | MEDLINE | ID: mdl-39113882
ABSTRACT
Endothelial dysfunction may contribute to pathogenesis of Takotsubo cardiomyopathy, but mechanism underlying endothelial dysfunction in the setting of catecholamine excess has not been clarified. The study reports that D1/D5 dopamine receptor signaling and small conductance calcium-activated potassium channels contribute to high concentration catecholamine induced endothelial cell dysfunction. For mimicking catecholamine excess, 100 µM epinephrine (Epi) was used to treat human cardiac microvascular endothelial cells. Patch clamp, FACS, ELISA, PCR, western blot and immunostaining analyses were performed in the study. Epi enhanced small conductance calcium-activated potassium channel current (ISK1-3) without influencing the channel expression and the effect was attenuated by D1/D5 receptor blocker. D1/D5 agonists mimicked the Epi effect, suggesting involvement of D1/D5 receptors in Epi effects. The enhancement of ISK1-3 caused by D1/D5 activation involved roles of PKA, ROS and NADPH oxidases. Activation of D1/D5 and SK1-3 channels caused a hyperpolarization, reduced NO production and increased ROS production. The NO reduction was membrane potential independent, while ROS production was increased by the hyperpolarization. ROS (H2O2) suppressed NO production. The study demonstrates that high concentration catecholamine can activate D1/D5 and SK1-3 channels through NADPH-ROS and PKA signaling and reduce NO production, which may facilitate vasoconstriction in the setting of catecholamine excess.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Transducción de Señal / Epinefrina / Especies Reactivas de Oxígeno / Células Endoteliales Límite: Humans Idioma: En Revista: Int J Med Sci Asunto de la revista: MEDICINA Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Australia
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Transducción de Señal / Epinefrina / Especies Reactivas de Oxígeno / Células Endoteliales Límite: Humans Idioma: En Revista: Int J Med Sci Asunto de la revista: MEDICINA Año: 2024 Tipo del documento: Article País de afiliación: China Pais de publicación: Australia