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Therefore, using an acute ex vivo model of hypothalamic and neurohypophyseal explants (obtained from male 6\/7\u2010week\u2010old Wistar rats) under conditions of extracellular iso\u2010 and hypertonicity, we determined the effects of NO<\/jats:styled-content> (600\u00a0\u03bcmol\u00a0L\u20101<\/jats:sup> sodium nitroprusside<\/jats:styled-content>), CO<\/jats:styled-content> (100\u00a0\u03bcmol\u00a0L\u20101<\/jats:sup> tricarbonylchloro[glycinato]ruthenium [II]) and H2<\/jats:sub>S (10\u00a0mmol\u00a0L\u20101<\/jats:sup> sodium sulphide) donors and nitric oxide synthase (NOS)<\/jats:styled-content> (300\u00a0\u03bcmol\u00a0L\u20101<\/jats:sup> N<\/jats:italic>\u03c9<\/jats:sub>\u2010methyl\u2010l<\/jats:sc>\u2010arginine [LNMMA]), haeme oxygenase (HO)<\/jats:styled-content> (200\u00a0\u03bcmol\u00a0L\u20101<\/jats:sup> Zn(II) deuteroporphyrin IX 2,4\u2010bis\u2010ethylene glycol [ZnDPBG]) and cystathionine \u03b2\u2010synthase (CBS<\/jats:styled-content>) (100\u00a0\u03bcmol\u00a0L\u20101<\/jats:sup> aminooxyacetate [AOA]) inhibitors on the release of hypothalamic ANP<\/jats:styled-content> and hypothalamic and neurohypophyseal AVP<\/jats:styled-content> and OT<\/jats:styled-content>, as well as on the activities of NOS<\/jats:styled-content>, HO<\/jats:styled-content> and CBS<\/jats:styled-content>. LNMMA<\/jats:styled-content> reversed hyperosmolality\u2010induced NOS<\/jats:styled-content> activity, and enhanced hormonal release by the hypothalamus and neurohypophysis, in addition to increasing CBS<\/jats:styled-content> and hypothalamic HO<\/jats:styled-content> activity. AOA<\/jats:styled-content> decreased hypothalamic and neurohypophyseal CBS<\/jats:styled-content> activity and hormonal release, whereas ZnDPBG<\/jats:styled-content> inhibited HO<\/jats:styled-content> activity and hypothalamic hormone release; however, in both cases, AOA<\/jats:styled-content> did not modulate NOS<\/jats:styled-content> and HO<\/jats:styled-content> activity and ZnDPBG<\/jats:styled-content> did not affect NOS<\/jats:styled-content> and CBS<\/jats:styled-content> activity. Thus, our data indicate that, although endogenous CO<\/jats:styled-content> and H2<\/jats:sub>S positively modulate AVP<\/jats:styled-content>, OT<\/jats:styled-content> and ANP<\/jats:styled-content> release, only NO<\/jats:styled-content> plays a concomitant role of modulator of hormonal release and CBS<\/jats:styled-content> activity in the hypothalamus and neurohypophysis and that of HO<\/jats:styled-content> activity in the hypothalamus during an acute osmotic stimulus, which suggests that NO<\/jats:styled-content> is a key gaseous controller of the neuroendocrine system.<\/jats:p>","DOI":"10.1111\/jne.12686","type":"journal-article","created":{"date-parts":[[2019,1,11]],"date-time":"2019-01-11T17:17:18Z","timestamp":1547227038000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":20,"title":["Nitric oxide acutely modulates hypothalamic and neurohypophyseal carbon monoxide and hydrogen sulphide production to control 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