Abstract
Plasma levels of the vasoconstrictor peptide endothelin-1 (ET-1) are elevated in salt sensitive hypertension. ET-1 induces superoxide generation in sympathetic ganglion neurons via an action on NAD(P)H oxidase. Superoxide anion levels are elevated in sympathetic neurons in hypertension. In this study, we tested the hypothesis that the increased NAD(P)H oxidase expression is the source of the increased ·O2·− in PC12 cells. Using western blotting, we measured the protein expression levels of NAD(P)H oxidase subunits p22phox, p47phox and the small GTPase rac-1 in one week NGF-differentiated PC12 cells treated with ET-1 (100nM) for 30minutes up to 7 days. ET-1 treatment increased protein expression of all of the NAD(P)H oxidase subunits compared with normal controls. The elevation of the protein expression peaked at 24 hours after the introduction of ET-1 to the culture medium. These data suggested that the elevation of · O2·−production observed in ET-1 treated PC12 cells are derived from the upregulation of NAD(P)H oxidase protein expression. This might reflect the role of neuronal NAD(P)H oxidase system in the sympathetic ganglion neurons’ ET-1 signaling in hypertension.
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 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.
