{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,5,13]],"date-time":"2024-05-13T04:31:39Z","timestamp":1715574699499},"reference-count":26,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2009,1,29]],"date-time":"2009-01-29T00:00:00Z","timestamp":1233187200000},"content-version":"vor","delay-in-days":394,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2008,1]]},"abstract":"<jats:sec><jats:title>Background and purpose:<\/jats:title><jats:p>In the setting of nitrate tolerance, endothelium\u2010dependent relaxation is reduced in several types of peripheral vessels. However, it is unknown whether chronic <jats:italic>in vivo<\/jats:italic> administration of nitroglycerine modulates such relaxation in cerebral arteries.<\/jats:p><\/jats:sec><jats:sec><jats:title>Experimental approach:<\/jats:title><jats:p>Isometric force and smooth muscle cell membrane potential were measured in endothelium\u2010intact strips from rabbit middle cerebral artery (MCA) and posterior cerebral artery (PCA).<\/jats:p><\/jats:sec><jats:sec><jats:title>Key results:<\/jats:title><jats:p>ACh (0.1\u201310\u2003\u03bc<jats:sc>M<\/jats:sc>) concentration\u2010dependently induced endothelium\u2010dependent relaxation during the contraction induced by histamine in both MCA and PCA. Chronic (10 days) <jats:italic>in vivo<\/jats:italic> administration of nitroglycerine reduced the ACh\u2010induced relaxation in PCA but not in MCA, in the presence of the cyclooxygenase inhibitor diclofenac (3\u2003\u03bc<jats:sc>M<\/jats:sc>). In the presence of the NO\u2010synthase inhibitor <jats:italic>N<\/jats:italic>\n<jats:sup>\u03c9<\/jats:sup>\u2010nitro\u2010<jats:sc>L<\/jats:sc>\u2010arginine (<jats:sc>L<\/jats:sc>\u2010NNA, 0.1\u2003m<jats:sc>M<\/jats:sc>) plus diclofenac, in MCA from both nitroglycerine\u2010untreated control and \u2010treated rabbits, ACh (0.1\u201310\u2003\u03bc<jats:sc>M<\/jats:sc>) induced a smooth muscle cell hyperpolarization and relaxation, and these were blocked by the small\u2010conductance Ca<jats:sup>2+<\/jats:sup>\u2010activated K<jats:sup>+<\/jats:sup>\u2010channel inhibitor apamin (0.1\u2003\u03bc<jats:sc>M<\/jats:sc>), but not by the large\u2010 and intermediate\u2010conductance Ca<jats:sup>2+<\/jats:sup>\u2010activated K<jats:sup>+<\/jats:sup>\u2010channel inhibitor charybdotoxin (0.1\u2003\u03bc<jats:sc>M<\/jats:sc>). In contrast, in PCA, ACh (&lt;3\u2003\u03bc<jats:sc>M<\/jats:sc>) induced neither hyperpolarization nor relaxation under these conditions, suggesting that the endothelium\u2010derived relaxing factor is NO in PCA, whereas endothelium\u2010derived hyperpolarizing factor (EDHF) plays a significant role in MCA.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions and implications:<\/jats:title><jats:p>It is suggested that in rabbit cerebral arteries, the function of the endothelium\u2010derived relaxing factor NO and that of EDHF may be modulated differently by chronic <jats:italic>in vivo<\/jats:italic> administration of nitroglycerine.<\/jats:p><jats:p><jats:italic>British Journal of Pharmacology<\/jats:italic> (2008) <jats:bold>153<\/jats:bold>, 132\u2013139; doi:<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" xlink:href=\"10.1038\/sj.bjp.0707562\">10.1038\/sj.bjp.0707562<\/jats:ext-link>; published online 29 October 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