{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,7]],"date-time":"2026-03-07T05:10:44Z","timestamp":1772860244170,"version":"3.50.1"},"reference-count":40,"publisher":"S. Karger AG","issue":"3-4","license":[{"start":{"date-parts":[[2016,1,1]],"date-time":"2016-01-01T00:00:00Z","timestamp":1451606400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"},{"start":{"date-parts":[[2016,1,1]],"date-time":"2016-01-01T00:00:00Z","timestamp":1451606400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/www.karger.com\/Services\/SiteLicenses"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Vasc Res"],"published-print":{"date-parts":[[2016]]},"abstract":"<b><i>Background\/Aim:<\/i><\/b> H<sub>2<\/sub>S is a novel vasoactivator. To verify the hypothesis that H<sub>2<\/sub>S may act as an endothelium-derived hyperpolarizing factor (EDHF) in the rat cerebrovasculature, the role of H<sub>2<\/sub>S in endothelium-derived relaxing factor (EDRF)-mediated responses was investigated. <b><i>Methods:<\/i><\/b> Cystathionine-&#x03B3;-lyase (CSE) was knocked down with an siRNA technique. Artery diameter, hyperpolarization and Ca<sup>2+<\/sup>-activated K<sup>+<\/sup> (K<sub>Ca<\/sub>) current were measured. <b><i>Results:<\/i><\/b> CSE knockdown was indicated by a decrease in protein and mRNA expression in the rat middle cerebral artery (MCA) and cerebral basilar artery (CBA). Acetylcholine (ACh) induced significant hyperpolarization and vasodilation in endothelium-intact MCA and CBA. Removal of the endothelium abolished these responses. The nitric oxide (NO) synthase inhibitor <smlcap>L<\/smlcap>-NAME, but not the PGI<sub>2<\/sub> production inhibitor indomethacin, significantly inhibited ACh-induced hyperpolarization and vasodilation in the CBA. In the presence of <smlcap>L<\/smlcap>-NAME and indomethacin, ACh-induced hyperpolarization and vasodilation in the MCA and CBA were attenuated. The non-NO\/PGI<sub>2<\/sub>-mediated responses were abolished by the K<sub>Ca<\/sub> channel blockers charybdotoxin and apamin. In the cerebral arteries from the CSE knockdown rat, non-NO\/PGI<sub>2<\/sub>-mediated responses were significantly attenuated, and the remaining responses were abolished by charybdotoxin and apamin or the CSE inhibitor propargylglycine. CSE knockdown did not affect <smlcap>L<\/smlcap>-NAME-sensitive responses in the CBA. Sodium hydrosulfide (NaHS) augmented the K<sub>Ca<\/sub> current in CBA vascular smooth muscle cells. <b><i>Conclusion:<\/i><\/b> EDHF-mediated responses in rat cerebral arteries were due to H<sub>2<\/sub>S activating the K<sub>Ca<\/sub> channel.<\/jats:p>","DOI":"10.1159\/000448712","type":"journal-article","created":{"date-parts":[[2016,10,12]],"date-time":"2016-10-12T21:01:37Z","timestamp":1476306097000},"page":"172-185","source":"Crossref","is-referenced-by-count":22,"title":["Involvement of Hydrogen Sulfide in Endothelium-Derived Relaxing Factor-Mediated Responses in Rat Cerebral 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