Abstract
Endothelin (ET) is a potent vasoconstrictor peptide, released from endothelial cells, which is associated with prostaglandin (PG) release. The mechanism by which ET causes the release of PG is not clearly understood. We used rat aortic endothelial cells to investigate the role of calcium (Ca 2+) in ET-1-induced prostacyclin (PGI 2) release. ET-1 (10 −9 M) produced a significant increase in PGI 2release. Pretreatment of rat aortic endothelial cells with different doses (10 −9 M and 10 −6M) of diltiazem (voltage-sensitive L-type calcium channel blocker) produced significant inhibition of ET-1- and PDBu-induced PGI 2release. Inhibition was first noted at 10 −9M and was complete at 10 −6M. Conversely, pretreatment of rat aortic endothelial cells with different doses (10 −9M and 10 −6M) of calcium channel blockers (thapsigargin, an intracellular calcium channel blocker or conotoxin, a voltage-sensitive N-type calcium channel blocker) produced no changes on ET-1- or PDBu-induced PGI 2release. These results provide further support for the concept that PKC mediates ET-induced PGI 2release in rat aortic endothelial cells via an increase in intracellular calcium and this increase is due to the influx of extracellular calcium and not to the release of calcium from the sarcoplasmic reticulum.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Prostaglandins, Leukotrienes and Essential Fatty Acids (PLEFA)
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
