{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T08:16:30Z","timestamp":1773303390334,"version":"3.50.1"},"reference-count":42,"publisher":"Institute of Physiology of the Czech Academy of Sciences","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Physiol Res"],"published-print":{"date-parts":[[2016,6,30]]},"abstract":"<jats:p>The purpose of the present study was to define the indirect central effect of hydrogen sulfide (H2S) on baroreflex control of sympathetic outflow. Perfusing the isolated carotid sinus with sodium hydrosulfide (NaHS), a H2S donor, the effect of H2S was measured by recording changes of renal sympathetic nerve activity (RSNA) in anesthetized male rats. Perfusion of isolated carotid sinus with NaHS (25, 50, 100 \u03bcmol\/l) dose and time-dependently inhibited sympathetic outflow. Preconditioning of glibenclamide (20 \u00b5mol\/l), a ATP-sensitive K+ channels (KATP) blocker, the above effect of NaHS was removed. With 1, 4-dihydro-2, 6-dimethyl-5-nitro-4-(2-[trifluoromethyl] phenyl) pyridine-3-carboxylic acid methyl ester (Bay K8644, 500 nmol\/l) pretreatment, which is an agonist of L-calcium channels, the effect of NaHS was eliminated. Perfusion of cystathionine \u03b3-lyase (CSE) inhibitor, DL-propargylglycine (PPG, 200 \u03bcmol\/l), increased sympathetic outflow. The results show that exogenous H2S in the carotid sinus inhibits sympathetic outflow. The effect of H2S is attributed to opening KATP channels and closing the L-calcium channels.<\/jats:p>","DOI":"10.33549\/physiolres.933050","type":"journal-article","created":{"date-parts":[[2020,2,21]],"date-time":"2020-02-21T08:29:16Z","timestamp":1582273756000},"page":"413-423","source":"Crossref","is-referenced-by-count":20,"title":["Perfusion of Isolated Carotid Sinus With Hydrogen Sulfide Attenuated the Renal Sympathetic Nerve Activity in Anesthetized Male Rats"],"prefix":"10.33549","author":[{"given":"Q.","family":"GUO","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Y.","family":"WU","sequence":"additional","affiliation":[{"name":"Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang, China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"H.","family":"XUE","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"L.","family":"XIAO","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S.","family":"JIN","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"R.","family":"WANG","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"19169","published-online":{"date-parts":[[2016,6,14]]},"reference":[{"key":"ref0","doi-asserted-by":"publisher","unstructured":"ABE K, KIMURA H: The possible role of hydrogen sulfide as an endogenous neuromodulator. 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