Szukana fraza: [Abstrakt = "Red blood cells \(RBC\) alterations and excessive activation of angiotensin \(Ang\)\-\(1– 12\)\/II pathway contribute to cardiovascular pathology, but their involvement in the development of peripheral endothelial dysfunction in heart failure \(HF\) remains unknown. Therefore, the aim of this PhD thesis was the following\: 1\) To describe the relationship between the development of peripheral endothelial dysfunction and RBCs alterations in HF 2\) To define the effect of exogenous Ang\-\(1–12\) and its conversion to Ang II on endothelial function in HF, focusing particularly on chymase and vascular\-derived thromboxane A2 \(TXA2\) involvement. In this study, a unique mouse model of chronic heart failure \(HF\) driven by cardiomyocyte\-specific overexpression of activated Gαq protein was used \(Tgαq\*44 mice\). In 8\-month\-old Tgαq\*44 mice, systemic endothelial dysfunction was detected as evidenced by a decreased acetylcholine\-induced vasodilation in the aorta in vivo, which was associated with impaired nitric oxide \(NO\) production, increased superoxide anion \(O2\- \) and increased eicosanoid production. Moreover, 8\-month\-old Tgαq\*44 mice showed significant structural RBC alterations, as well as increased RBC stiffness. Erythropathy in 12\-month\-old Tgαq\*44 mice involved significantly altered RBC shape and increased elasticity, increased red cell distribution width \(RDW\), poor"]

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