{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,10,14]],"date-time":"2023-10-14T15:39:27Z","timestamp":1697297967709},"reference-count":69,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2009,1,29]],"date-time":"2009-01-29T00:00:00Z","timestamp":1233187200000},"content-version":"vor","delay-in-days":3011,"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":[[2000,11]]},"abstract":"<jats:p>\n<jats:list list-type=\"explicit-label\">\n<jats:list-item>\n<jats:p>Relaxing effect of loop diuretics, piretanide and furosemide in comparison with acetylcholine (ACh) was investigated in guinea\u2010pig isolated mesenteric resistance arteries.<\/jats:p>\n<\/jats:list-item>\n<jats:list-item>\n<jats:p>Concentration\u2010response curves to ACh (0.001\u201310\u2003\u03bc<jats:sc>M<\/jats:sc>) and diuretics (0.0001\u20131\u2003\u03bc<jats:sc>M<\/jats:sc>) were constructed in noradrenaline (10\u201330\u2003\u03bc<jats:sc>M<\/jats:sc>)\u2010precontracted arteries incubated either in normal physiological salt solution (PSS) or in 30\u2003m<jats:sc>M<\/jats:sc> KCl PSS (K\u2010PSS).<\/jats:p>\n<\/jats:list-item>\n<jats:list-item>\n<jats:p>In PSS, maximal relaxations (R<jats:sub>max<\/jats:sub>) and pD<jats:sub>2<\/jats:sub> to ACh were 87\u00b12% and 7.1\u00b10.1 (<jats:italic>n<\/jats:italic>=10). <jats:sc>L<\/jats:sc>\u2010N<jats:sup>G<\/jats:sup>\u2010nitro\u2010arginine methyl ester (<jats:sc>L<\/jats:sc>\u2010NAME, 100\u2003\u03bc<jats:sc>M<\/jats:sc>) reduced R<jats:sub>max<\/jats:sub> by 20% (<jats:italic>P<\/jats:italic>&lt;0.01, <jats:italic>n<\/jats:italic>=7) and pD<jats:sub>2<\/jats:sub> by 10% (<jats:italic>P<\/jats:italic>&lt;0.01). In contrast, indomethacin (10\u2003\u03bc<jats:sc>M<\/jats:sc>) increased R<jats:sub>max<\/jats:sub> by 19% (<jats:italic>P<\/jats:italic>&lt;0.01, <jats:italic>n<\/jats:italic>=8) and pD<jats:sub>2<\/jats:sub> by 10% (<jats:italic>P<\/jats:italic>&lt;0.05). Combination of <jats:sc>L<\/jats:sc>\u2010NAME+indomethacin reversed the effect observed with either of these inhibitors used alone. In K\u2010PSS, R<jats:sub>max<\/jats:sub> was attenuated by 40% (<jats:italic>P<\/jats:italic>&lt;0.001, <jats:italic>n<\/jats:italic>=6) compared to PSS. <jats:sc>L<\/jats:sc>\u2010NAME reduced R<jats:sub>max<\/jats:sub> by 65% (<jats:italic>P<\/jats:italic>&lt;0.01, <jats:italic>n<\/jats:italic>=5) and increased pD<jats:sub>2<\/jats:sub> by 15 fold. <jats:sc>L<\/jats:sc>\u2010NAME+indomethacin suppressed the resistant relaxation.<\/jats:p>\n<\/jats:list-item>\n<jats:list-item>\n<jats:p>In PSS+<jats:sc>L<\/jats:sc>\u2010NAME+indomethacin, inhibitors of small (SK<jats:sub>Ca<\/jats:sub>; apamin, 0.1\u2003\u03bc<jats:sc>M<\/jats:sc>) and large (BK<jats:sub>Ca<\/jats:sub>; iberiotoxin and charybdotoxin, 0.1\u2003\u03bc<jats:sc>M<\/jats:sc>) conductance Ca<jats:sup>2+<\/jats:sup>\u2010sensitive K<jats:sup>\u2212<\/jats:sup>\u2010channels used alone had little effect on the ACh\u2010response. Combination of apamin+iberiotoxin reduced R<jats:sub>max<\/jats:sub> by 40% (<jats:italic>P<\/jats:italic>&lt;0.05, <jats:italic>n<\/jats:italic>=7) while apamin+charybdotoxin fully abolished the resistant relaxation.<\/jats:p>\n<\/jats:list-item>\n<jats:list-item>\n<jats:p>In PSS, piretanide and furosemide induced relaxation with R<jats:sub>max<\/jats:sub>: 89\u00b13% vs 84\u00b15% and pD<jats:sub>2<\/jats:sub>: 8.5\u00b10.1 vs 7.7\u00b10.2 (<jats:italic>P<\/jats:italic>&lt;0.01) for piretanide (<jats:italic>n<\/jats:italic>=11) and furosemide (<jats:italic>n<\/jats:italic>=10), respectively. Endothelial abrasion suppressed relaxation to diuretics. <jats:sc>L<\/jats:sc>\u2010NAME and indomethacin used alone or in combination did not significantly modify the response to diuretics.<\/jats:p>\n<\/jats:list-item>\n<jats:list-item>\n<jats:p>In K\u2010PSS, piretanide\u2010induced relaxation was abolished whereas that to furosemide was reduced by 70% (<jats:italic>P<\/jats:italic>&lt;0.001, <jats:italic>n<\/jats:italic>=9) compared to PSS and was suppressed by <jats:sc>L<\/jats:sc>\u2010NAME+indomethacin. In PSS+<jats:sc>L<\/jats:sc>\u2010NAME+indomethacin, apamin slightly reduced relaxation to diuretics whereas charybdotoxin or iberiotoxin abolished the response.<\/jats:p>\n<\/jats:list-item>\n<jats:list-item>\n<jats:p>These results indicate that ACh\u2010evoked relaxation is mediated by both NO\/PGl<jats:sub>2<\/jats:sub>\u2010dependent and \u2010independent mechanisms. The EDHF\u2010dependent component relies on activation of Ca<jats:sup>2+<\/jats:sup>\u2010activated K<jats:sup>+<\/jats:sup> channels, is sensitive to a combination of apamin+charybdotoxin and to a smaller degree to a combination of apamin+iberiotoxin. Loop diuretic\u2010induced relaxation is endothelium\u2010dependent, appears to be mediated by NO, PGl<jats:sub>2<\/jats:sub> and EDHF for furosemide and EDHF only for piretanide. For the two diuretics, opening of BK<jats:sub>Ca<\/jats:sub> channels may be involved in the relaxation.<\/jats:p>\n<\/jats:list-item>\n<\/jats:list>\n<\/jats:p><jats:p><jats:italic>British Journal of Pharmacology<\/jats:italic> (2000) <jats:bold>131<\/jats:bold>, 1211\u20131219; doi:<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" xlink:href=\"10.1038\/sj.bjp.0703693\">10.1038\/sj.bjp.0703693<\/jats:ext-link><\/jats:p>","DOI":"10.1038\/sj.bjp.0703693","type":"journal-article","created":{"date-parts":[[2005,1,28]],"date-time":"2005-01-28T21:00:40Z","timestamp":1106946040000},"page":"1211-1219","update-policy":"http:\/\/dx.doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Role of EDHF in the vasodilatory effect of loop diuretics in guinea\u2010pig mesenteric resistance arteries"],"prefix":"10.1111","volume":"131","author":[{"given":"Fabrice","family":"Pourageaud","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Catherine","family":"Bappel\u2010Gozalbes","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Roger","family":"Marthan","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jean\u2010Louis","family":"Freslon","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2009,1,29]]},"reference":[{"key":"e_1_2_6_2_1","first-page":"423","article-title":"Varying extracellular [K+]; a functional approach to separating EDHF\u2010 and EDNO\u2010related mechanisms in perfused rat mesenteric arterial bed","volume":"21","author":"ADEAGBO A.S.O","year":"1993","journal-title":"Cardiovasc. 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