Omeprazole suppresses endothelial calcium response and eNOS Ser1177 phosphorylation in porcine aortic endothelial cells.
Animals
Aorta
/ cytology
Bradykinin
/ metabolism
Calcium
/ metabolism
Dose-Response Relationship, Drug
Endoplasmic Reticulum
/ drug effects
Endothelial Cells
/ drug effects
Endothelium, Vascular
/ cytology
Epoprostenol
/ metabolism
Nitric Oxide
/ metabolism
Nitric Oxide Synthase Type III
/ metabolism
Omeprazole
/ pharmacology
Phosphorylation
Swine
Calcium
Endothelial cells
Endothelium-dependent relaxing factors
Nitric oxide synthase
Omeprazole
Journal
Molecular biology reports
ISSN: 1573-4978
Titre abrégé: Mol Biol Rep
Pays: Netherlands
ID NLM: 0403234
Informations de publication
Date de publication:
Jul 2021
Jul 2021
Historique:
received:
11
02
2021
accepted:
12
07
2021
pubmed:
23
7
2021
medline:
7
1
2022
entrez:
22
7
2021
Statut:
ppublish
Résumé
Although high doses of proton pump inhibitors can elicit an anticancer effect, this strategy may impair vascular biology. In particular, their effects on endothelial Ca Omeprazole (10-1000 μM) suppressed both bradykinin (BK)- and thapsigargin-induced endothelial Ca Our results are the first to indicate that high doses of omeprazole may suppress both store-operated Ca
Sections du résumé
BACKGROUND
BACKGROUND
Although high doses of proton pump inhibitors can elicit an anticancer effect, this strategy may impair vascular biology. In particular, their effects on endothelial Ca
METHODS AND RESULTS
RESULTS
Omeprazole (10-1000 μM) suppressed both bradykinin (BK)- and thapsigargin-induced endothelial Ca
CONCLUSION
CONCLUSIONS
Our results are the first to indicate that high doses of omeprazole may suppress both store-operated Ca
Identifiants
pubmed: 34291395
doi: 10.1007/s11033-021-06561-0
pii: 10.1007/s11033-021-06561-0
doi:
Substances chimiques
Nitric Oxide
31C4KY9ESH
Epoprostenol
DCR9Z582X0
Nitric Oxide Synthase Type III
EC 1.14.13.39
Omeprazole
KG60484QX9
Bradykinin
S8TIM42R2W
Calcium
SY7Q814VUP
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
5503-5511Subventions
Organisme : Hamamatsu University School of Medicine
ID : 42351T 1013511
Organisme : Hamamatsu University School of Medicine
ID : 42351T 1013522
Informations de copyright
© 2021. The Author(s), under exclusive licence to Springer Nature B.V.
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