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The present study was designed to investigate the downstream molecular mechanism of salusin\u2010<jats:italic>\u03b2<\/jats:italic> in the <jats:styled-content style=\"fixed-case\">PVN<\/jats:styled-content> in hypertension.<\/jats:p><\/jats:sec><jats:sec><jats:title>Method<\/jats:title><jats:p>Renovascular hypertension was induced by two\u2010kidney, one\u2010clip (2K1C) in male <jats:styled-content style=\"fixed-case\">SD<\/jats:styled-content> rats. Acute experiments were carried out 4\u00a0weeks after 2K1C or sham operation under anaesthesia.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>MrgA1 <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> expression and salusin\u2010<jats:italic>\u03b2<\/jats:italic> level in the PVN as well as plasma salusin\u2010<jats:italic>\u03b2<\/jats:italic> level were increased in 2K1C rats. Bilateral PVN microinjection of salusin\u2010<jats:italic>\u03b2<\/jats:italic> increased the RSNA, MAP and HR in 2K1C rats, which were abolished by the pre\u2010treatment with polyethylene glycol\u2013superoxide dismutase (PEG\u2010SOD), the superoxide anion scavenger tempol, the NAD(P)H oxidase inhibitor apocynin or the protein kinase C (PKC) inhibitor chelerythrine chloride (CLC), but not affected by the AT<jats:sub>1<\/jats:sub> receptor antagonist losartan, the Mas receptor antagonist A\u2010779, the NOS inhibitor L\u2010NAME or the GABA<jats:sub>A<\/jats:sub> and GABA<jats:sub>B<\/jats:sub> receptor antagonists gabazine+CGP\u201035348. Salusin\u2010<jats:italic>\u03b2<\/jats:italic>\u2010induced increases in superoxide anion level and NAD(P)H oxidase activity in the PVN were abolished by the PVN pre\u2010treatment with CLC. Salusin\u2010<jats:italic>\u03b2<\/jats:italic> increased AVP levels in rostral ventrolateral medulla and plasma, which were prevented by the pre\u2010treatment with PEG\u2010SOD, apocynin or CLC in 2K1C rats. Salusin\u2010<jats:italic>\u03b2<\/jats:italic> augmented the enhanced activity of PKC in the PVN in 2K1C rats.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Protein kinase C\u2010<jats:styled-content style=\"fixed-case\">NAD<\/jats:styled-content>(P)H oxidase\u2010superoxide anions pathway in the <jats:styled-content style=\"fixed-case\">PVN<\/jats:styled-content> is involved in salusin\u2010<jats:italic>\u03b2<\/jats:italic>\u2010induced sympathetic activation, pressor response and <jats:styled-content style=\"fixed-case\">AVP<\/jats:styled-content> release in renovascular hypertension.<\/jats:p><\/jats:sec>","DOI":"10.1111\/apha.12188","type":"journal-article","created":{"date-parts":[[2013,10,28]],"date-time":"2013-10-28T16:36:59Z","timestamp":1382978219000},"page":"534-545","source":"Crossref","is-referenced-by-count":29,"title":["Superoxide anions involved in sympathoexcitation and pressor effects of salusin\u2010<i>\u03b2<\/i> in paraventricular 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