ISSN:
1474-8673
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Chemistry and Pharmacology
,
Medicine
Notes:
1 The relationship between the effects of endogenous nitric oxide (NO) and prostanoids on the noradrenaline (NA)-induced contractions and the mechanisms involved were investigated in the rat perfused mesenteric bed, using NG-nitro-l-arginine methyl ester (l-NAME), a NO synthase inhibitor and sodium nitroprusside (SNP), a NO donor.2 The constrictor responses to NA were reduced to 50% by the cyclooxygenase inhibitor 10 μm indomethacin as well as by 1 μm SNP. When indomethacin and SNP were perfused simultaneously the contractions were further reduced.3 The NA-induced contractions were increased by the addition of 400 μml-NAME and the addition of either indomethacin or SNP abolished such increases. The simultaneous perfusion of both agents further reduced the contractions.4 Removal of the endothelium increased NA-induced contractions to a similar extent as l-NAME and this increase was abolished by indomethacin as well as by SNP.5 The perfusion of 10 μm NA augmented the release of prostaglandin (PG) F2α by the mesenteric bed without modifications in any other prostanoid. In the presence of l-NAME, this effect was further increased. However, SNP abolished the NA-induced stimulation of PGF2α release.6 In de-endothelialized preparations NA also stimulated PGF2α production as observed in intact preparations. This effect was more marked in the presence of l-NAME; in contrast, SNP abolished the stimulation.7 In conclusion, the present results suggest an opposite action between NO and PGF2α on the NA-induced contractions in the rat mesenteric bed.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1046/j.1474-8673.2003.00292.x
