MedicGo
Extracellular Ca2+ promotes nitric oxide production via Ca2+-sensing receptor-Gq/11 protein-endothelial nitric oxide synthase signaling in human vascular endothelial cells.
Metadata
Journaljournal of pharmacological sciences2.835Date
2019 Jun 22
a year ago
Type
Journal Article
Volume
2020-Aug / 143 : 315-319
Author
Horinouchi T 1, Mazaki Y 2, Terada K 3, Miwa S 2
Affiliation
  • 2. Department of Cellular Pharmacology, Graduate School of Medicine, Hokkaido University, North 15, West 7, Kita-ku, Sapporo-City, Hokkaido, 060-8638, Japan.
  • 3. Department of Biochemistry and Molecular Biology, Shiga University of Medical Science, Seta Tsukinowa-cho, Otsu-City, Shiga, 520-2192, Japan.
Doi
PMIDMESH
Calcium
Cells, Cultured
Endothelial Cells
GTP-Binding Protein alpha Subunits, Gq-G11
Humans
Nitric Oxide
Nitric Oxide Synthase
Receptors, Calcium-Sensing
Signal Transduction
Abstract
This study examined the possible involvement of Ca2+-sensing receptor (CaSR) in nitric oxide (NO) production in human vascular endothelial cells. Extracellular Ca2+ elevated the intracellular Ca2+ concentration, the endothelial NO synthase (eNOS) phosphorylation level, and NO release from the cells. These responses were inhibited by a CaSR antagonist and a Gq/11 protein inhibitor. Application of an endothelial cell suspension induced vasorelaxation in isolated rat thoracic aorta precontracted by phenylephrine. Adding an NO scavenger to the organ bath abolished this vasorelaxation response. These results suggest that extracellular Ca2+ promotes NO generation via CaSR- and Gq/11 protein-mediated eNOS activation.
Keywords: Ca(2+)-sensing receptor Endothelial nitric oxide synthase Extracellular Ca(2+)
Fav
Like
Download
Share
Export
Cite
2.8
J Pharmacol Scijournal of pharmacological sciences
Metadata
LocationJapan
FromJAPANESE PHARMACOLOGICAL SOC

No Data

© 2017 - 2020 Medicgo
Powered by some medical students