[SIN-1 interactions with the generation of cyclic nucleotides and arachidonate oxide metabolites in the uterine muscle].
In the uterine smooth muscle, SIN-1 stimulated cGMP accumulation independently of the presence of Ca2+ and activated the soluble form of guanylate-cyclase through mechanisms apparently similar to those involved in the stimulations evoked by NO-containing compounds. These activations appear different from those induced by hydroperoxy-unsaturated fatty acids and which contribute to the carbachol-mediated cGMP accumulation. SIN-1 did not influence the rise in cAMP of the biosynthesis of PG1(2) and 12-HETE due to exogenous arachidonic acid. By contrast, SIN-1 markedly inhibited the increased synthesis of PG1(2) induced by the ionophore A23187 which was due to a prior, Ca2+-dependent, liberation of endogenous arachidonic acid. The data suggests an interference of SIN-1 with the generation and/or the expression of the Ca2+ signal.
D000818:Animals; D001095:Arachidonic Acids / Q000494:pharmacology*; D000242:Cyclic AMP / Q000378:metabolism*; D006152:Cyclic GMP / Q000378:metabolism*; D011464:Epoprostenol / Q000378:metabolism; D005260:Female; D006162:Guanylate Cyclase / Q000378:metabolism*; D006168:Guinea Pigs; D008981:Molsidomine / Q000031:analogs & derivatives* / Q000494:pharmacology; D009215:Myometrium / Q000378:metabolism*
D001095:Arachidonic Acids; C002385:linsidomine; D008981:Molsidomine; D011464:Epoprostenol; D000242:Cyclic AMP; D006162:Guanylate Cyclase; D006152:Cyclic GMP
Interactions du SIN-1 avec la génération des nucléotides cycliques et des métabolites oxydés de l'arachidonate dans le muscle utérin.