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Acta Physiologica Sinica ; (6): 581-590, 2018.
Artigo em Inglês | WPRIM | ID: wpr-777227

RESUMO

Fructose intake has increased dramatically over the past century and the upward trend has continued until recently. Increasing evidence suggests that the excessive intake of fructose induces salt-sensitive hypertension. While the underlying mechanism is complex, the kidney likely plays a major role. This review will highlight recent advances in the renal mechanisms of fructose-induced salt-sensitive hypertension, including (pro)renin receptor-dependent activation of intrarenal renin-angiotensin system, increased nephron Na transport activity via sodium/hydrogen exchanger 3 and Na/K/2Cl cotransporter, increased renal uric acid production, decreased renal nitric oxide production, and increased renal reactive oxygen species production, and suggest actions based on these mechanisms that have therapeutic implications.


Assuntos
Humanos , Pressão Sanguínea , Frutose , Hipertensão , Rim , Óxido Nítrico , Metabolismo , Espécies Reativas de Oxigênio , Metabolismo , Sistema Renina-Angiotensina , Cloreto de Sódio na Dieta , Trocador 3 de Sódio-Hidrogênio , Metabolismo , Ácido Úrico , Metabolismo
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