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The present study evaluated whether Na<jats:sup>+<\/jats:sup>in the paraventricular nucleus (PVN) causes larger pressor responses in Dahl S (SS\/Mcw) than R (Dahl SS.BN13) rats and whether mineralocorticoid receptors, benzamil-blockable Na<jats:sup>+<\/jats:sup>channels, \u201couabain,\u201d angiotensin type 1 receptors, or NO mediates these enhanced responses. Na<jats:sup>+<\/jats:sup>-rich aCSF in the PVN caused 30\u201340% larger increases in blood pressure and heart rate in Dahl S than R or Wistar rats, whereas responses to ouabain, ANG II, or N<jats:sup>\u03c9<\/jats:sup>-nitro-l-arginine methyl ester hydrochloride (l-NAME) in the PVN were the same. These responses to Na<jats:sup>+<\/jats:sup>were not affected by eplerenone, benzamil, or Fab fragments, whereas they were fully blocked by losartan, in Dahl S and R rats. l-NAME enhanced them more in Dahl R than S rats, thereby equalizing the responses in the two strains. Pressor responses to l-NAME in the PVN were attenuated by a high-salt diet in Dahl S, but not R, rats. The results indicate that acute and chronic increases in Na<jats:sup>+<\/jats:sup>concentration in the PVN inhibit NO release in the PVN of Dahl S, but not R, rats, thereby contributing to the enhanced pressor responses to Na<jats:sup>+<\/jats:sup>in Dahl S rats.<\/jats:p>","DOI":"10.1152\/ajpregu.00246.2011","type":"journal-article","created":{"date-parts":[[2011,7,28]],"date-time":"2011-07-28T02:27:56Z","timestamp":1311820076000},"page":"R1338-R1349","source":"Crossref","is-referenced-by-count":17,"title":["Mechanisms mediating sodium-induced pressor responses in the PVN of Dahl rats"],"prefix":"10.1152","volume":"301","author":[{"given":"Alexander","family":"Gabor","sequence":"first","affiliation":[{"name":"Hypertension Unit, University of Ottawa Heart Institute, Ottawa, Ontario, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Frans H. 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