Year-end Sale % OFF 
Abstract
The effect of Endothelin-3 on phosphoinositide turnover was studied in two brain structures, the subfornical organ and median eminence. ET-3 increased inositol monophosphate accumulation in the range 1 nM to 2 μM. Basal and stimulated InsP 1 accumulation increased linearly during 1 h. The PI response elicited by ET-3 was dependent on the presence of extracellular Ca ++. Removal of extracellular Ca ++ or addition of Cd ++ resulted in a marked decrease in ET-3-stimulated InsP1 accumulation. On the contrary, phosphoinositide hydrolysis was not changed by the calcium channel blockers nifedipine or amlodipine; however, it was decreased by amiloride, a Na +/H + antiporter or Na +/Ca ++ exchange blocker. ET-3 induced PI breakdown was inhibited in, a dose-dependent manner, by neomycin, an inhibitor of phospholipase C. These findings further support the hypothesis that stimulation of PI turnover constitutes one of the signalling pathways of ET-3 in the central nervous system, possibly through the stimulation of a specific receptor coupled to phospholipase C.
Published Version
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 callDisclaimer: 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.
