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Cardiovasc Pathol ; 24(4): 224-9, 2015.
Artículo en Inglés | MEDLINE | ID: mdl-25659450

RESUMEN

Hypertension is the most common risk factor for various cardiovascular and cerebrovascular diseases that affects approximately 61 million, or 25% of the population in United States. The dietary salt intake is one of the most important but modifiable factors for hypertension. In the current study, we aim to elucidate the role of aquaporin 1 in high-salt-induced hypertension and cardiac injuries and whether angiotensin II receptor blocker valsartan could ameliorate the effect of high salt on blood pressure. Mice were fed with normal diet, high-salt diet in the presence or absence of valsartan for 4 weeks. The body weight gain, feeding behavior, blood pressure, and cardiac pathology changes were monitored after 4 weeks. The expression of aquaporin 1, vascular endothelial growth factor, transforming growth factor ß1, and basic fibroblast growth factor were analyzed using quantitative real-time polymerase chain reaction, Western blot, and immunohistochemical staining. Valsartan partially reversed the effects of high-salt diet on hypertension, cardiac injuries such as fibrosis and inflammatory cell infiltration, and inhibition of aquaporin 1 and angiogenic factors; valsartan alone did not exert such effects. The current data demonstrated that the reduction of cardiac aquaporin 1 and angiogenic factor expression level might be associated with high-salt-induced hypertension and cardiac injuries in mice, which could be ameliorated by angiotensin II receptor blocker treatment.


Asunto(s)
Proteínas Angiogénicas/metabolismo , Bloqueadores del Receptor Tipo 1 de Angiotensina II/farmacología , Antihipertensivos/farmacología , Acuaporina 1/metabolismo , Cardiopatías/prevención & control , Hipertensión/tratamiento farmacológico , Miocitos Cardíacos/efectos de los fármacos , Cloruro de Sodio Dietético , Valsartán/farmacología , Proteínas Angiogénicas/genética , Animales , Acuaporina 1/genética , Presión Sanguínea/efectos de los fármacos , Citocinas/metabolismo , Citoprotección , Modelos Animales de Enfermedad , Conducta Alimentaria/efectos de los fármacos , Fibrosis , Cardiopatías/etiología , Cardiopatías/genética , Cardiopatías/metabolismo , Cardiopatías/patología , Cardiopatías/fisiopatología , Hipertensión/etiología , Hipertensión/metabolismo , Hipertensión/fisiopatología , Masculino , Ratones Endogámicos C57BL , Miocitos Cardíacos/metabolismo , Miocitos Cardíacos/patología , Factores de Tiempo , Aumento de Peso/efectos de los fármacos
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