Publication:  The relaxant effect of vasoactive intestinal polypeptide in the isolated canine uterine artery: The role of endothelium
Loading...
Date
2004
Journal Title
Journal ISSN
Volume Title
Publisher
Abstract
The purpose of this study was to examine the effect of vasoactive intestinal polypeptide (VIP) on the uterine artery obtained from non-pregnant dogs. VIP (3 × 10                             -9                             -3 × 10                             -7                              M) induced concentration-dependent relaxation in canine uterine arteries with intact endothelium, pre-contracted with 10                             -5                              M phenylephrine (pEC                              50                              = 7.52 ± 0.02, maximal response was 82.19 ± 2.15%, n = 36). The administration of the cyclooxygenase inhibitor indomethacin (10                              -5                              M) or 4-aminopyridine (4-AP), a blocker of potassium channels (10                             -5                              M), did not modify the relaxation induced by VIP. Contrary to this, N                             G                             -nitro-L-arginine (L-NOARG) (10                             -5                              M) inhibited relaxation is evoked by VIP. Indomethacin applied with L-NOARG did not provoke further inhibition of VIP-induced relaxation. In the presence of both L-NOARG and L-NOARG + indomethacin, 4-AP led to the further inhibition of VIP-induced relaxation of canine uterine artery. It is concluded that VIP induces endothelium-dependent relaxation of uterine arteries of non-pregnant dogs, which can be entirely explained by the production of nitric oxide (NO) from the endothelial cells. We proposed that when NO synthesis is inhibited, VIP induces further relaxation, independent of the edothelium-derived relaxing factors, probably through activation of K                             +                              channels. © 2004 Blackwell Verlag.
