Abstract
We analyzed functional changes in activities of NO and EDHF in mice aorta from ApoE/LDLR−/− mice and Tgαq*44 mice that represent a model of atherosclerosis and heart failure, respectively. Progression of atherosclerosis and progression of heart failure was also quantified. In thoracic aorta from apoE/LDLR−/− mice acetylcholine (Ach)-induced endothelium-dependent relaxation was already impaired in 2-month-old apoE/LDLR−/− mice and remained diminished in older apoE/LDLR−/− mice. Importantly, EDHF-mediated relaxation (inhibited by miconazol and TEA) was gradually upregulated in apoE/LDLR−/− mice parallel to the progression of atherosclerosis. In turn, in thoracic aorta from Tgαq*44 mice Ach-induced endothelium-dependent relaxation in thoracic aorta was preserved in 7-month-old Tgαq*44 mice while it was impaired in 14-month-old Tgαq*44 mice. Basal NO activity and SNAP-induced endothelium-independent relaxation remained unchanged in Tgαq*44 mice irrespectively to the age of animals. Finally, EDHF-mediated pathway was not upregulated in Tgαq*44 mice.
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