Amelioration of AngiotensinII-induced salt-sensitive hypertension by L-FABP in proximal tubules

最近的研究表明，肾内肾素-血管紧张素系统(RAS)的不适当激活导致了活性氧的产生，这可能是盐敏感型高血压的原因之一。另一方面，L-FABP在人类肾脏近端小管中表达，可能起到内源性抗氧化作用。本研究旨在观察L提取液对盐敏感型高血压的抗氧化作用。提示近端肾小管L-FABP对血管紧张素转换酶诱导的肾性高血压有保护作用，并可抑制肾内RAS活性，减轻氧化应激。因此，近端肾小管L-FABP可能在SSHT中起一定的病理作用。

Recent findings indicated that inappropriate activation of the intrarenal renin-angiotensin system(RAS) induces reactive oxygen species production, which may contribute to salt-sensitive hypertension. On the other hand, L-FABP is expressed in renal proximal tubules in humans and may play an endogenous antioxidant role. The present study is to examine the antioxidative effect of L-FABP on salt-sensitive hypertension. The present findings indicated that L-FABP in proximal tubules may protect against AngII-induced SSHT in combination with attenuation of intrarenal RAS activation, oxidative stress. Therefore, L-FABP of proximal tubules may play a pathological role in SSHT.