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home:starting:physician:reluctant [04.30.2019] – [Specific research] sallieq | home:starting:physician:reluctant [06.01.2019] – [Specific research] sallieq | ||
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- | Olmesartan significantly reduced myocardial infarct size and improved LV contractility at a dose (3 mg/kg) with systemic vasodilating effects but not at a lower dose (0.3 mg/kg) without hemodynamic effects.(in rat)(({{pubmed> | + | Olmesartan significantly reduced myocardial infarct size and improved LV contractility at a dose (3 mg/kg) with systemic vasodilating effects but not at a lower dose (0.3 mg/kg) without hemodynamic effects.[in rat](({{pubmed> |
Inhibition of renin-angiotensin system attenuates periadventitial inflammation and reduces atherosclerotic lesion formation. (({{pubmed> | Inhibition of renin-angiotensin system attenuates periadventitial inflammation and reduces atherosclerotic lesion formation. (({{pubmed> | ||
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- | 6 mg/kg olmesartan reduces the inflammatory process and bone loss in rats (({{pubmed> | + | 6 mg/kg olmesartan reduces the inflammatory process and bone loss [in rats] (({{pubmed> |
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+ | Olmesartan at a dose of 10 mg/kg prevented the mucosal damage and inflammation associated with 5-FU-induced OM, increasing granulation and tissue repair. [in hamsters] (({{pubmed> | ||
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OLM substantially delayed the development of left ventricular remodeling in type 2 diabetes (({{pubmed> | OLM substantially delayed the development of left ventricular remodeling in type 2 diabetes (({{pubmed> | ||
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+ | we investigated the effects of RNH-6270, an active metabolite of olmesartan, on TNF-α-induced human glomerular EC (HGEC) damage to clarify the renoprotective mechanisms of ARBs. Our findings suggested that olmesartan might have protective effects against TNF-α-induced glomerular EC dysfunction.(({{pubmed> | ||
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+ | We orally administered olmesartan 1, 3, and 10 mg/kg/day to rats with EAM for 3 weeks. The cardioprotection of olmesartan may be due to suppression of inflammatory cytokines dependent of the hemodynamic modifications. | ||
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+ | AlphaTau1 receptor blockers, olmesartan and valsartan (10(-9)-10(-6) mol/L) showed a significant reduction on TNF-alpha-induced LDH and NAG release in human renal proximal tubular epithelial cells (({{pubmed> | ||
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+ | These data added to our previous results further provide a mechanistic rationale for olmesartan' | ||
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