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Roles and mechanisms of dopamine receptor signaling in catecholamine excess induced endothelial dysfunctions: research paper

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 potassi...

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Hauptverfasser: Yang, Zhen (VerfasserIn) , Li, Yingrui (VerfasserIn) , Huang, Mengying (VerfasserIn) , Li, Xin (VerfasserIn) , Fan, Xuehui (VerfasserIn) , Yan, Chen (VerfasserIn) , Meng, Zenghui (VerfasserIn) , Liao, Bin (VerfasserIn) , Hamdani, Nazha (VerfasserIn) , Yang, Xiaoli (VerfasserIn) , Zhou, Xiao-Bo (VerfasserIn) , El-Battrawy, Ibrahim (VerfasserIn) , Akın, Ibrahim (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: 2024.07.22
In: International journal of medical sciences
Year: 2024, Jahrgang: 21, Heft: 10, Pages: 1964-1975
ISSN:1449-1907
DOI:10.7150/ijms.96550
Online-Zugang:Verlag, kostenfrei, Volltext: https://doi.org/10.7150/ijms.96550
Verlag, kostenfrei, Volltext: https://www.medsci.org/v21p1964.htm
Volltext
Verfasserangaben:Zhen Yang, Yingrui Li, Mengying Huang, Xin Li, Xuehui Fan, Chen Yan, Zenghui Meng, Bin Liao, Nazha Hamdani, Xiaoli Yang, Xiaobo Zhou, Ibrahim El-Battrawy and Ibrahim Akin
Beschreibung
Zusammenfassung: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.
Beschreibung:Gesehen am 28.10.2024
Beschreibung:Online Resource
ISSN:1449-1907
DOI:10.7150/ijms.96550

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