SUMMARY
In the first part of this study we examined and compared mechanisms of the red wine (RW) induced vasorelaxation in guinea pig (GP) and rat aorta.
Acetylcholine-induced relaxation of norepinephrine-precontracted aortic rings was stronger in rat than in GP aorta while RW-induced vasorelaxation was stronger in GP aorta. L-nitro arginine methyl ester (L-NAME) abolished RW-induced vasorelaxation in rat aorta, while in GP aorta it was only reduced by 50%. To examine mechanisms of the L-NAME-resistant relaxation, GP aortic rings were additionally exposed to indomethacin, clotrimazole, and their combination. Indomethacin insignificantly reduced RW-induced relaxation, but in combination with L-NAME the relaxation was synergistically decreased
(80%). After clotrimazole the relaxation was reduced by 25% and addition of indomethacin caused no further reduction.
Only the combination of L-NAME, indomethacin, and clotrimazole prevented RW-induced vasorelaxation. RW-induced vasorelaxation in KCl-precontracted GP rings was significantly smaller (Emax 78.31±6.09%) than the relaxation induced by RW in norepinephrineprecontracted rings (Emax 126.01±2.11%). L-NAME in KCl-precontracted GP rings prevented RW-induced vasorelaxation.
In conclusion, different pathways are involved in the RW- induced vasorelaxation in GP aorta, in contrast to rat aorta, in which NO plays main role.