Search for: [Abstract = "RBC deformability and elevated oxidative stress \(gluthatione \(GSH\)\/glutathione disulfide \(GSSG\) ratio\). Inhibition of arginase reversed endothelial dysfunction induced by RBCs isolated from Tgαq\*44 mice, ex vivo model of RBCsendothelial interaction in the isolated aorta. Ang\-\(1–12\) induced endothelial dysfunction in 4\- and 12\- month\-old Tgαq\*44 mice, was associated with increased Ang II generation, which was not inhibited by chymostatin, a chymase inhibitor. Moreover, TXA2 generation was upregulated in response to Ang\-\(1\-12\) or Ang II in aortic rings isolated from 12\-month\-old Tgαq\*44 mice, but not from 4\-month\-old Tgαq\*44 mice. Furthermore, the adverse effects of Ang\-\(1–12\) and Ang II on endotheliumdependent vasodilation in the aorta were inhibited by TXA2 receptor antagonist \(SQ 29548\) or Ang receptor type I antagonist \(losartan\) in 12\-month\-old\-Tgαq\*44 mice, but these antagonists remained without effects in 4\-month\-old\- Tgαq\*44 mice. Altogether in this Ph.D. thesis it was demonstrated that in the Tgαq\*44 murine model of HF, erythropathy involving structural and biochemical alterations, upregulated arginase as well as overactivity of intravascular Ang\-\(1–12\)\/Ang II\/TXA2 pathway may contribute to the development endothelial dysfunction in the aorta. Accordingly, RBC arginase and intravascular Ang\-\(1–12\)\/Ang II\/TXA2 pathways may represent a novel t"]

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