El consumo excesivo de sal como riesgo de enfermedad renal : efectos sobre la expresión fisiopatológica de moléculas relacionadas con daño renal
The objective was to demonstrate that acute and/or chronic sodium chloride overload causes renal and vascular inflammation, which is evidenced by the overexpression of inflammatory and fibrotic markers. Male Sprague-Dawley rats were acutely infused with hypertonic saline solution or fed a hypersodic...
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| Formato: | Tesis doctoral acceptedVersion |
| Lenguaje: | Español |
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Facultad de Farmacia y Bioquímica
2018
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| Acceso en línea: | http://repositoriouba.sisbi.uba.ar/gsdl/cgi-bin/library.cgi?a=d&c=posgraafa&cl=CL1&d=HWA_3138 http://repositoriouba.sisbi.uba.ar/gsdl/collect/posgraafa/index/assoc/HWA_3138.dir/3138.PDF |
| Aporte de: |
| Sumario: | The objective was to demonstrate that acute and/or chronic sodium chloride overload causes renal and vascular inflammation, which is evidenced by the overexpression of inflammatory and fibrotic markers. Male Sprague-Dawley rats were acutely infused with hypertonic saline solution or fed a hypersodic diet for 3 weeks, with and without treatment with the AT1 receptor blocker (AT1R) losartan or tempol (oxidative stress inhibitor). Acute sodium overload increased the reabsorptive work in the proximal tubules, generating relative hypoxia by over-expressing renal HIF-? and ANP as adaptive mechanisms. The hypertensive component of the local renin angiotensin system was activated with overexpression of angiotensin II, AT1R and NF-kB, whereas the vasodepressant and antiinflammatory components were inhibited (ECA2-Ang (1-7)MasR axis, AT2R and eNOS), increasing the release of proinflammatory cytokines and chemokines (TGF-1?), pro-fibrotic (?-SMA) and oxidative stress. Saline overload decreased the expression of AQP1 and AQP2, inhibiting water transport in renal tubules and favoring inflammation. If the acute overload becomes chronic through a hypersodic diet, renal inflammation is followed by chronic fibrosis, processes that are prevented, attenuated or reversed by blocking AT1R with losartan or inhibiting oxidative stress with tempol. |
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