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The present study investigated whether NCX was affected by prostacyclin and nitric oxide (NO) released from the vascular endothelium, as NCX contains phosphorylation sites for PKA and PKG.<\/jats:p><\/jats:sec><jats:sec><jats:title>Experimental approach:<\/jats:title><jats:p>Rat aortic rings were set up in organ baths. Tension was measured across the ring with a force transducer.<\/jats:p><\/jats:sec><jats:sec><jats:title>Key results:<\/jats:title><jats:p>Lowering extracellular [Na+] ([Na+]<jats:sub>o<\/jats:sub>) to 1.18\u2003m<jats:sc>M<\/jats:sc>induced vasoconstriction in rat endothelium\u2010denuded aortic rings. This effect was blocked by the NCX inhibitor KB\u2010R7943 (2\u20102\u2010[4\u2010(4\u2010nitrobenzyloxy)phenyl] ethyl isothiourea methanesulphonate; 1\u2003\u03bc<jats:sc>M<\/jats:sc>). In endothelium\u2010intact aortic rings, decreasing [Na+]<jats:sub>o<\/jats:sub>did not constrict the aortic rings significantly, but after treatment with the guanylate cyclase inhibitor ODQ (1<jats:italic>H<\/jats:italic>\u2010[1,2,4]oxadiazolo[4,3\u2010a]quinoxalin\u20101\u2010one; 1\u2003\u03bc<jats:sc>M<\/jats:sc>) or the NOS inhibitor<jats:sc>L<\/jats:sc>\u2010NAME (<jats:italic>N<\/jats:italic><jats:sup>\u03c9<\/jats:sup>\u2010nitro\u2010L\u2010arginine methyl ester; 50\u2003\u03bc<jats:sc>M<\/jats:sc>), a vasoconstriction that was similar in size to that in endothelium\u2010denuded preparations was evident. The vasorelaxation induced by the NO donor sodium nitroprusside sodium nitroprusside dihydrate (30\u2003n<jats:sc>M<\/jats:sc>) was the same in the endothelium\u2010denuded aortic rings preconstricted with either low Na<jats:sup>+<\/jats:sup>(1.18\u2003m<jats:sc>M<\/jats:sc>), the thromboxane A2 agonist U46619 (9,11\u2010dideoxy\u20109\u03b1, 11\u03b1\u2010methanoepoxy prostaglandin F<jats:sub>2\u03b1<\/jats:sub>; 0.1\u2003\u03bc<jats:sc>M<\/jats:sc>) or high K<jats:sup>+<\/jats:sup>(80\u2003m<jats:sc>M<\/jats:sc>).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions and implications:<\/jats:title><jats:p>The results suggest that the endothelium inhibits NCX operation via guanylate cyclase\/NO. This is stronger than for other constrictors such as phenylephrine and may relate to concomitant NCX\u2010stimulated NO release from the endothelium. This finding may be important where NCX operates in reverse mode, such as during ischaemia, and highlights a new mechanism whereby the endothelium modulates Ca<jats:sup>2+<\/jats:sup>homoeostasis in vascular smooth muscle.<\/jats:p><jats:p><jats:italic>British Journal of Pharmacology<\/jats:italic>(2008)<jats:bold>154<\/jats:bold>, 982\u2013990; doi:<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" xlink:href=\"10.1038\/bjp.2008.178\">10.1038\/bjp.2008.178<\/jats:ext-link>; published online 12 May 2008<\/jats:p><\/jats:sec>","DOI":"10.1038\/bjp.2008.178","type":"journal-article","created":{"date-parts":[[2008,5,12]],"date-time":"2008-05-12T10:03:36Z","timestamp":1210586616000},"page":"982-990","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Endothelial nitric oxide attenuates Na<sup>+<\/sup>\/Ca<sup>2+<\/sup>exchanger\u2010mediated vasoconstriction in rat 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