Roles and Mechanisms of Dopamine Receptor Signaling in Catecholamine Excess Induced Endothelial Dysfunctions.
Humans
Signal Transduction
/ drug effects
Epinephrine
Endothelial Cells
/ metabolism
Reactive Oxygen Species
/ metabolism
Nitric Oxide
/ metabolism
Catecholamines
/ metabolism
Small-Conductance Calcium-Activated Potassium Channels
/ metabolism
Endothelium, Vascular
/ metabolism
Cyclic AMP-Dependent Protein Kinases
/ metabolism
NADPH Oxidases
/ metabolism
Receptors, Dopamine D5
/ metabolism
Receptors, Dopamine D1
/ metabolism
Receptors, Dopamine
/ metabolism
Takotsubo syndrome
dopamine receptor
endothelial dysfunction, nitric oxide.
small conductance calcium-activated potassium channel
Journal
International journal of medical sciences
ISSN: 1449-1907
Titre abrégé: Int J Med Sci
Pays: Australia
ID NLM: 101213954
Informations de publication
Date de publication:
2024
2024
Historique:
received:
23
03
2024
accepted:
03
07
2024
medline:
8
8
2024
pubmed:
8
8
2024
entrez:
8
8
2024
Statut:
epublish
Résumé
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 (I
Identifiants
pubmed: 39113882
doi: 10.7150/ijms.96550
pii: ijmsv21p1964
pmc: PMC11302566
doi:
Substances chimiques
Epinephrine
YKH834O4BH
Reactive Oxygen Species
0
Nitric Oxide
31C4KY9ESH
Catecholamines
0
Small-Conductance Calcium-Activated Potassium Channels
0
Cyclic AMP-Dependent Protein Kinases
EC 2.7.11.11
NADPH Oxidases
EC 1.6.3.-
Receptors, Dopamine D5
137750-35-7
Receptors, Dopamine D1
0
Receptors, Dopamine
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1964-1975Informations de copyright
© The author(s).
Déclaration de conflit d'intérêts
Competing Interests: The authors have declared that no competing interest exists.