Role of hydrogen sulfide in heparin-induced vasodilatory response in rat aorta

Objective: The aim of the project is to determine the role and contribution of hydrogen sulfide in the relaxation effect of non-fractional heparin in the vessel as a new target. The aim is not only to determine whether hydrogen sulfide is present under the relaxing effect of heparin, but also to compare it with other relaxation mechanisms and to determine the contribution rate. Method: In the experiments, the relaxation responses of the vessels obtained from 9-12 weeks old Wistar rats and in the endothelial intact and non-endothelial preparations were investigated. Carbdotoxin with L-NAME (10-4 M), L-NAME (10-4) and indomethacin (10-5 M), blockers of structural and inducible nitric oxide synthase (NOS) isoforms of abdominal aorta rings precontracted with phenylephrine (10-7 M), apamine (10-7 M) combination, cumulative heparin concentrations and relaxation responses were determined. Also; AOAA- (2x10-3M), before and after incubation, heparin (0.5-6U / ml), similar to L-NAME, indomethacin, apamine / caribdotoxin next to the different combinations of AOAA added with the cumulative concentrations of heparin again in the contracted vessel preparation relaxation responses were obtained and compared. Results: Heparin in two tissues with intact endothelium and endothelium damaged; especially in endothelial damaged vascular preparations. It is seen that the relaxation response decreases after incubating with CBS enzyme inhibitor AOAA in H2S production. It is seen that the relaxation response decreases after incubating with CBS enzyme inhibitor AOAA in H2S production. After the incubation with L-NAME, the relaxing effect of heparin in FE contracted tissue is not completely eliminated. Compared to the decrease in the relaxation response seen by AOAA incubation and the decrease in the presence of indomethacin, it is seen that H2S is involved in more heparin relaxant mechanism than prostaglandins. Conclusion: Heparin produces relaxation response in rat aorta depending on concentration. This relaxation mechanism appears to be involved in H2S. H2S performs this relaxation, possibly through other potassium channels, mainly through KATP potassium channels. Key words: Heparin, hydrogen sulfide, vasorelaxation