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home:starting:physician:reluctant [06.01.2019] – [Specific research] sallieq | home:starting:physician:reluctant [06.01.2019] – [Specific research] sallieq | ||
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Olmesartan attenuated CTGF induction, reduced perivascular fibrosis and ameliorated cardiac dysfunction in a PO heart. Our results provide insight into the beneficial effects of olmesartan on PO hearts, independent of blood-pressure lowering. [in rat] (({{pubmed> | Olmesartan attenuated CTGF induction, reduced perivascular fibrosis and ameliorated cardiac dysfunction in a PO heart. Our results provide insight into the beneficial effects of olmesartan on PO hearts, independent of blood-pressure lowering. [in rat] (({{pubmed> | ||
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+ | Olmesartan treatment reversed virtually all neuroendocrine and histopathological cardiac changes induced by EAM (We used experimental autoimmune myocarditis in rats) (({{pubmed> | ||
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+ | Treatment with ARB prevents the progression of peritoneal fibrosis and suppresses expression of adhesion molecules in the peritoneum. (({{pubmed> | ||
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+ | ( in cultured human renal proximal tubular cells) Olmesartan inhibited the effect of costimulation with ANG II and IL-6 on AGT expression, indicating that AT1R is critical for AGT enhancement by ANG II. Moreover, IL-6R antibody also neutralized the effect, suggesting that these agents exert a synergistic effect, even though they do not independently induce human AGT expression. These findings suggest that AT1R blockers may attenuate the secondary pathophysiological effects of ANG II even though ANG II alone does not exert any direct effects, and this may partially account for the powerful renoprotective effects of AT1R blocker beyond its depressor effect. (({{pubmed> | ||
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+ | Olmesartan treatment had already significantly reduced serum levels of high-sensitivity C-reactive protein (-15.1%; P<0.05), high-sensitivity tumor necrosis factor-alpha (-8.9%; P<0.02), interleukin-6 (-14.0%; P<0.05), and monocyte chemotactic protein-1 (-6.5%; P<0.01) after 6 weeks of therapy, whereas placebo treatment (ie, blood pressure reduction) had no major effect on inflammation markers. (({{pubmed> | ||
Long term treatment Data suggest 40 & 80 mg olmesartan are able to significantly remodel & destiffen the arterial wall material during long-term treatment, partly independently of blood pressure, compared with 20 mg. hyper.ahajournals.org/ | Long term treatment Data suggest 40 & 80 mg olmesartan are able to significantly remodel & destiffen the arterial wall material during long-term treatment, partly independently of blood pressure, compared with 20 mg. hyper.ahajournals.org/ |