Abstract
Previous studies showed that O2 sensing by the carotid body (CB) requires carbon monoxide (CO) generation by heme oxygenase (HO)‐2 and hydrogen sulfide (H2S) synthesis by cystathionine‐γ‐lyase (CSE). However, the mechanism(s) underlying O2‐dependent gaseous messenger generation are not known. Here, we report that CO but not H2S generation is sensitive to changes in O2 levels. The O2‐dependent CO generation requires two cysteine residues (C265 and C282) located in the heme‐regulatory motif of HO‐2. Carbon monoxide, in turn inhibits H2S generation from CSE via protein kinase G (PKG)‐dependent phosphorylation of serine 377. Hypoxia, by reducing CO generation, decreases the inhibition of CSE resulting in elevated H2S, which mediates the increased CB neural activity. These results demonstrate that PKG‐dependent regulation of H2S governs O2 sensing by the carotid body (Supported by NIH‐HLBI PO1 HL‐090554).
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.
