{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T12:12:17Z","timestamp":1787314337809,"version":"build-2736575974"},"reference-count":48,"publisher":"American Physiological Society","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Regulatory, Integrative and Comparative Physiology"],"published-print":{"date-parts":[[2016,6,1]]},"abstract":"<jats:p>\n                    The present study was designed to explore the role of soluble guanylate cyclase (sGC)\/cyclic guanosine monophosphate (cGMP)\/PKG pathway in sulfur dioxide (SO\n                    <jats:sub>2<\/jats:sub>\n                    )-induced vasodilation. We showed that SO\n                    <jats:sub>2<\/jats:sub>\n                    induced a concentration-dependent relaxation of phenylephrine (PE)-precontracted rat aortic rings in association with an increase in cGMP concentration, whereas l-aspartic acid \u03b2-hydroxamate (HDX), an inhibitor of SO\n                    <jats:sub>2<\/jats:sub>\n                    synthase, contracted rings in a dose-dependent manner. Pretreatment of aortic rings with the sGC inhibitor ODQ (30 \u03bcM) attenuated the vasodilatory effects of SO\n                    <jats:sub>2<\/jats:sub>\n                    , suggesting the involvement of cGMP pathway in SO\n                    <jats:sub>2<\/jats:sub>\n                    -induced vasodilation. Mechanistically, SO\n                    <jats:sub>2<\/jats:sub>\n                    upregulated the protein levels of sGC and PKG dimers, while HDX inhibited it, indicating SO\n                    <jats:sub>2<\/jats:sub>\n                    could promote cGMP synthesis through sGC activation. Furthermore, the dimerization of sGC and PKG and vasodilation induced by SO\n                    <jats:sub>2<\/jats:sub>\n                    in precontracted rings were significantly prevented by thiol reductants dithiothreitol (DTT). In addition, SO\n                    <jats:sub>2<\/jats:sub>\n                    reduced the activity of phosphodiesterase type 5 (PDE5), a cGMP-specific hydrolytic enzyme, implying that SO\n                    <jats:sub>2<\/jats:sub>\n                    elevated cGMP concentration by inhibiting its hydrolysis. Hence, SO\n                    <jats:sub>2<\/jats:sub>\n                    exerted its vasodilatory effects at least partly by promoting disulfide-dependent dimerization of sGC and PKG, resulting in an activated sGC\/cGMP\/PKG pathway in blood vessels. These findings revealed a new mode of action and mechanisms by which SO\n                    <jats:sub>2<\/jats:sub>\n                    regulated the vascular tone.\n                  <\/jats:p>","DOI":"10.1152\/ajpregu.00101.2015","type":"journal-article","created":{"date-parts":[[2016,3,24]],"date-time":"2016-03-24T00:38:37Z","timestamp":1458779917000},"page":"R1073-R1080","source":"Crossref","is-referenced-by-count":26,"title":["The vasodilatory effect of sulfur dioxide via SGC\/cGMP\/PKG pathway in association with sulfhydryl-dependent dimerization"],"prefix":"10.1152","volume":"310","author":[{"given":"Qiuyu","family":"Yao","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Peking University First Hospital, Beijing, People's Republic of China;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yaqian","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Peking University First Hospital, Beijing, People's 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