{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,8]],"date-time":"2026-05-08T20:58:09Z","timestamp":1778273889525,"version":"3.51.4"},"reference-count":39,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2009,12,16]],"date-time":"2009-12-16T00:00:00Z","timestamp":1260921600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Physiology"],"published-print":{"date-parts":[[2010,2]]},"abstract":"<jats:p>The regulation of blood pressure and sympathetic outflow by the brain renin\u2013angiotensin system in animals subjected to raised or lowered dietary Na<jats:sup>+<\/jats:sup>intake is unclear. This study compared the mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) responses to intracerebroventricular (<jats:sc>i.c.v<\/jats:sc>.) infusion of angiotensin II (AngII) and III (AngIII) before and after peripheral V<jats:sub>1<\/jats:sub>receptor blockade (V<jats:sub>1<\/jats:sub>B) in \u03b1\u2010chloralose\u2013urethane\u2010anaesthetized rats fed a low (0.03%, LNa<jats:sup>+<\/jats:sup>), normal (0.3%, NNa<jats:sup>+<\/jats:sup>) or high Na<jats:sup>+<\/jats:sup>diet (3.0%, HNa<jats:sup>+<\/jats:sup>) from 4 to 11 weeks of age. The rise in MAP 2 min post AngII<jats:sc>i.c.v<\/jats:sc>. was greater in HNa<jats:sup>+<\/jats:sup>(14 \u00b1 3 mmHg)<jats:italic>versus<\/jats:italic>LNa<jats:sup>+<\/jats:sup>(8 \u00b1 1 mmHg,<jats:italic>P<\/jats:italic>&lt; 0.05) and after AngIII<jats:sc>i.c.v<\/jats:sc>. in HNa<jats:sup>+<\/jats:sup>(14 \u00b1 3 mmHg)<jats:italic>versus<\/jats:italic>NNa<jats:sup>+<\/jats:sup>(6 \u00b1 1 mmHg,<jats:italic>P<\/jats:italic>&lt; 0.05) and LNa<jats:sup>+<\/jats:sup>(7 \u00b1 1 mmHg,<jats:italic>P<\/jats:italic>&lt; 0.05). The MAP responses to AngII and AngIII<jats:sc>i.c.v<\/jats:sc>. were abolished after V<jats:sub>1<\/jats:sub>B in LNa<jats:sup>+<\/jats:sup>, but were only attenuated in HNa<jats:sup>+<\/jats:sup>. In NNa<jats:sup>+<\/jats:sup>, V<jats:sub>1<\/jats:sub>B blunted the MAP responses to AngII and abolished those to AngIII. The MAP remained elevated 30 min after AngII in all groups, but returned to baseline levels 15 min after AngIII in NNa<jats:sup>+<\/jats:sup>and HNa<jats:sup>+<\/jats:sup>(<jats:italic>P<\/jats:italic>&lt; 0.01). Twenty minutes after<jats:sc>i.c.v<\/jats:sc>. AngII, RSNA rose above baseline in HNa<jats:sup>+<\/jats:sup>(112 \u00b1 1%), a response not observed in the LNa<jats:sup>+<\/jats:sup>and NNa<jats:sup>+<\/jats:sup>groups. Twenty minutes post AngIII<jats:sc>i.c.v<\/jats:sc>., RSNA was elevated in both HNa (109 \u00b1 2%) and NNa<jats:sup>+<\/jats:sup>(109 \u00b1 2%). After V<jats:sub>1<\/jats:sub>B, RSNA rose only in the HNa<jats:sup>+<\/jats:sup>group 15 min post AngIII infusion (109 \u00b1 1%). Together, these findings: (1) suggest that HNa<jats:sup>+<\/jats:sup>intake augments the MAP and RSNA responses to<jats:sc>i.c.v<\/jats:sc>. AngII and AngIII; (2) highlight an important role for peripheral V<jats:sub>1<\/jats:sub>receptors during these responses; and (3) differentiate the effects of AngII and AngIII on blood pressure and RSNA.<\/jats:p>","DOI":"10.1113\/expphysiol.2009.049833","type":"journal-article","created":{"date-parts":[[2009,10,31]],"date-time":"2009-10-31T00:55:38Z","timestamp":1256950538000},"page":"282-295","source":"Crossref","is-referenced-by-count":13,"title":["Influence of dietary sodium on the blood pressure and renal sympathetic nerve activity responses to intracerebroventricular angiotensin II and angiotensin III in anaesthetized rats"],"prefix":"10.1113","volume":"95","author":[{"given":"Belinda L.","family":"Houghton","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chunlong","family":"Huang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Edward 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