Search for: [Abstract = "Endothelial dysfunction \(ED\) is a hallmark of heart failure \(HF\). Clinically, most cases of HF is due to CAD. On the other hand, ED is seen in patient with severe HF of non\-ischemic origin. Mechanisms leading to the development of secondary type of ED are still not clear. Aim of the present study was to describe the development of secondary type of coronary ED in Tg\[alfa\]q\*44 mice as well as to elucidate the involvement of aldosterone in this phenomenon. Both coronary endothelium\-dependent and endothelium\-independent responses were assessed in isolated Tg\[alfa\]q\*44 hearts and age\-matched FVB mice. In addition, level of 6\-keto\-PGF1\[alfa\] in cardiac effluent and production of 02\- in cardiac tissue were assessed. Despite increased generation of O2\- in cardiac tissue, endothelial function was not altered in Tg\[alfa\]q\*44 mice at the age of 4 months. However, coronary ED developed, as evidenced by impaired NO\-induced but not PGI2\-induced vasodilatation in Tg\[alfa\]q\*44 mice at the age of 14 months. Interestingly, there was a compensatory increase in basal PGI2 production in Tg\[alfa\]q\*44 hearts. Treatment of Tg\[alfa\]q\*44 mice with canrenone, aldosteron receptor antagonist improved both survival and NO\-mediated vasodilatation in Tg\[alfa\]q\*44 mice but had no effects on heart hypertrophy, pulmonary congestion and basal PGI2 production. In conclusion, development of coronary ED is secondary to cardiomyocytes pathology in Tg\[alfa\]q\*44 mice and is characterized by decreased NO bioavailability and compensatory increase in PGI2 production in coronary circulation. Development of secondary type of coronary ED in Tg\[alfa\]q\*44 mice is at last partly related to aldosterone in Tg\[alfa\]q\*44 mice."]

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