Efectos de las infusiones sistémicas de angiotensina II sobre la rama ascendente gruesa del Asa de Henle

Increases in the Renin-Angiotensin system contribute to the development of salt-sensitive hypertension (SSH). This condition affects 50% of hypertensive patients. The pharmacological strategies aimed at decreasing blood pressure by reducing the synthesis of Ang II or by blocking its specific recepto...

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Autor principal: González Vicente, Agustín
Otros Autores: Dominici, Fernando P.
Formato: Tesis doctoral acceptedVersion
Lenguaje:Español
Publicado: 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_2394
http://repositoriouba.sisbi.uba.ar/gsdl/collect/posgraafa/index/assoc/HWA_2394.dir/2394.PDF
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Sumario:Increases in the Renin-Angiotensin system contribute to the development of salt-sensitive hypertension (SSH). This condition affects 50% of hypertensive patients. The pharmacological strategies aimed at decreasing blood pressure by reducing the synthesis of Ang II or by blocking its specific receptor AT1 are less effective in these patients, so are commonly combined with a diuretic. This suggests that patients with SSH have an increased renal reabsorption of sodium and fluids. The thick ascending limb (TAL) of the loop of Henle reabsorbs -30% of the sodium filtered through the glomerulus, and is crucial in the generation of the osmotic gradient necessary for water reabsorption by collecting ducts. Epidemiological and animal studies suggest that the TAL participates in the development of SSH. The results obtained in this thesis shows that 1-week infusion of Ang II raises the activity of the Na+/K+-ATPase in the TAL. In addition, Ang II decreases the production of the NO in response to natriuretic stimuli. In conclusion, during Ang II-induced hypertension, the net transport of Na+ in the TAL is increased, possibly by a reduction in the NO-signaling pathway. These changes can reduce the excretion of Na+ and contribute to the sensitivity of blood pressure to salt intake.