{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T09:16:33Z","timestamp":1773306993018,"version":"3.50.1"},"reference-count":31,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2016,1,1]]},"abstract":"<jats:p>Hydrogen sulfide (H<jats:sub>2<\/jats:sub>S) has emerged as an important gasotransmitter in the vasculature. In this study, we tested the hypothesis that H<jats:sub>2<\/jats:sub>S contributes to coronary vasoregulation and evaluated the physiological relevance of two sources of H<jats:sub>2<\/jats:sub>S, namely, cystathionine-\u03b3-lyase (CSE) and 3-mercaptypyruvate sulfertransferase (MPST). MPST was detected in human coronary artery endothelial cells as well as rat and mouse coronary artery; CSE was not detected in the coronary vasculature. Rat coronary artery homogenates produced H<jats:sub>2<\/jats:sub>S through the MPST pathway but not the CSE pathway in vitro. In vivo coronary vasorelaxation response was similar in CSE knockout mice, wild-type mice (WT), and WT mice treated with the CSE inhibitor propargylglycine, suggesting that CSE-produced H<jats:sub>2<\/jats:sub>S does not have a significant role in coronary vasoregulation in vivo. Ex vivo, the MPST substrate 3-mercaptopyruvate (3-MP) and H<jats:sub>2<\/jats:sub>S donor sodium hydrosulfide (NaHS) elicited similar coronary vasoreactivity responses. Pyruvate did not have any effects on vasoreactivity. The vasoactive effect of H<jats:sub>2<\/jats:sub>S appeared to be nitric oxide (NO) dependent: H<jats:sub>2<\/jats:sub>S induced coronary vasoconstriction in the presence of NO and vasorelaxation in its absence. Maximal endothelial-dependent relaxation was intact after 3-MP and NaHS induced an increase in preconstriction tone, suggesting that endothelial NO synthase activity was not significantly inhibited. In vitro, H<jats:sub>2<\/jats:sub>S reacted with NO, which may, in part explain the vasoconstrictive effects of 3-MP and NaHS. Taken together, these data show that MPST rather than CSE generates H<jats:sub>2<\/jats:sub>S in coronary artery, mediating its effects through direct modulation of NO. This has important implications for H<jats:sub>2<\/jats:sub>S-based therapy in healthy and diseased coronary arteries.<\/jats:p>","DOI":"10.1152\/ajpheart.00574.2014","type":"journal-article","created":{"date-parts":[[2015,10,31]],"date-time":"2015-10-31T02:49:06Z","timestamp":1446259746000},"page":"H71-H79","source":"Crossref","is-referenced-by-count":48,"title":["MPST but not CSE is the primary regulator of hydrogen sulfide production and function in the coronary artery"],"prefix":"10.1152","volume":"310","author":[{"given":"Maggie M.","family":"Kuo","sequence":"first","affiliation":[{"name":"Department of Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dae Hee","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland;"},{"name":"Department of Anethesiology and Pain Medicine, Ajou University School of Medicine, Suwon, Korea"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sandeep","family":"Jandu","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yehudit","family":"Bergman","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Siqi","family":"Tan","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Huilei","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Deepesh R.","family":"Pandey","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Theodore P.","family":"Abraham","sequence":"additional","affiliation":[{"name":"Department of Medicine (Cardiology), Johns Hopkins University, Baltimore, Maryland; 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