{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T14:30:43Z","timestamp":1790605843882,"version":"4.1.0"},"reference-count":39,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2009,1,29]],"date-time":"2009-01-29T00:00:00Z","timestamp":1233187200000},"content-version":"vor","delay-in-days":2769,"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":[[2001,7]]},"abstract":"<jats:p>\n<jats:list list-type=\"explicit-label\">\n<jats:list-item><jats:p>Inhaled nitric oxide (iNO) is widely used in the treatment of pulmonary hypertension while inhaled NO donors have been suggested as an alternative therapy. The differential susceptibility to inactivation by oxidative stress and oxyhaemoglobin of NO and two NO donors, sodium nitroprusside (SNP) and S\u2010nitroso\u2010N\u2010acetyl\u2010penicillamine (SNAP) were analysed in isolated endothelium\u2010denuded pulmonary arteries from 2\u2010week\u2010old piglets stimulated with U46619.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>NO, SNAP and SNP relaxed the arteries (pIC<jats:sub>30<\/jats:sub>=7.73\u00b10.12, 7.26\u00b10.17 and 6.43\u00b10.13, respectively) but NO was not detected electrochemically in the bath after the addition of SNP and only at concentrations at which SNAP produced more than 50% relaxation.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>The sGC inhibitor ODQ (10<jats:sup>\u22126<\/jats:sup>\u2003<jats:sc>M<\/jats:sc>) or the sarcoplasmic Ca<jats:sup>2+<\/jats:sup>\u2010ATPase thapsigargin (2\u00d710<jats:sup>\u22126<\/jats:sup>\u2003<jats:sc>M<\/jats:sc>) markedly inhibited the relaxation induced by NO, SNAP and SNP.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Addition of oxyhaemoglobin (3\u00d710<jats:sup>\u22127<\/jats:sup>\u2003<jats:sc>M<\/jats:sc>) or diethyldithiocarbamate (1\u2003m<jats:sc>M<\/jats:sc>) markedly inhibited NO\u2010 (pIC<jats:sub>30<\/jats:sub>=6.88\u00b10.07 and 6.92\u00b10.18, respectively), weakly inhibited SNAP\u2010 and had no effect on SNP\u2010induced relaxation. Xanthine oxidase (5\u2003mu\u2003ml<jats:sup>\u22121<\/jats:sup>) plus hypoxanthine (10<jats:sup>\u22124<\/jats:sup>\u2003<jats:sc>M<\/jats:sc>) markedly inhibited NO\u2010 (pIC<jats:sub>30<\/jats:sub>=6.96\u00b10.12) but not SNAP\u2010 or SNP\u2010induced relaxation.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Superoxide dismutase (SOD), MnCl<jats:sub>2<\/jats:sub>, diphenileneiodonium and exposing the luminal surface of the rings outwards (inversion) potentiated the relaxant responses of NO (pIC<jats:sub>30<\/jats:sub>=8.52\u00b10.16, 8.23\u00b10.11, 8.01\u00b10.11 and 8.20\u00b10.10, respectively). However, SOD did not modify the NO detected by the electrode and had no effect on SNAP\u2010 or SNP\u2010induced relaxation.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Therefore, the kinetics and local distribution of NO release of NO donors influence the susceptibility to the scavenging effects of oxyhaemoglobin and superoxide.<\/jats:p><\/jats:list-item>\n<\/jats:list>\n<\/jats:p><jats:p><jats:italic>British Journal of Pharmacology<\/jats:italic> (2001) <jats:bold>133<\/jats:bold>, 615\u2013624; doi:<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" xlink:href=\"10.1038\/sj.bjp.0704103\">10.1038\/sj.bjp.0704103<\/jats:ext-link><\/jats:p>","DOI":"10.1038\/sj.bjp.0704103","type":"journal-article","created":{"date-parts":[[2005,1,28]],"date-time":"2005-01-28T21:31:17Z","timestamp":1106947877000},"page":"615-624","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":24,"title":["Nitric oxide\u2010 and nitric oxide donors\u2010induced relaxation and its modulation by oxidative stress in piglet pulmonary arteries"],"prefix":"10.1111","volume":"133","author":[{"given":"Jos\u00e9 Gustavo","family":"L\u00f3pez\u2010L\u00f3pez","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Francisco","family":"P\u00e9rez\u2010Vizca\u00edno","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Angel L","family":"Cogolludo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Manuel","family":"Ibarra","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Francisco","family":"Zaragoz\u00e1\u2010Arn\u00e1ez","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Juan","family":"Tamargo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2009,1,29]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1990.259.6.H1921"},{"key":"e_1_2_7_3_1","doi-asserted-by":"crossref","first-page":"435","DOI":"10.1152\/jappl.1998.84.2.435","article-title":"Pulmonary vasodilation by nitric oxide gas and prodrug aerosols in acute pulmonary hypertension","volume":"8","author":"ADRIE C.","year":"1998","journal-title":"J. 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