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Renal amino acid transport systems and essential hypertension

机译:肾氨基酸输送系统和原发性高血压

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Several clinical and animal studies suggest that “blood pressure goes with the kidney,” that is, a normotensive recipient of a kidney genetically programmed for hypertension will develop hypertension. Intrarenal dopamine plays an important role in the pathogenesis of hypertension by regulating epithelial sodium transport. The candidate transport systems for L-DOPA, the source for dopamine, include the sodium-dependent systems B0, B0,+, and y+L, and the sodium-independent systems L (LAT1 and LAT2) and b0,+. Renal LAT2 is overexpressed in the prehypertensive spontaneously hypertensive rat (SHR), which might contribute to enhanced L-DOPA uptake in the proximal tubule and increased dopamine production, as an attempt to overcome the defect in D1 receptor function. On the other hand, it has been recently reported that impaired arginine transport contributes to low renal nitric oxide bioavailability observed in the SHR renal medulla. Here we review the importance of renal amino acid transporters in the kidney and highlight pathophysiological changes in the expression and regulation of these transporters in essential hypertension. The study of the regulation of renal amino acid transporters may help to define the underlying mechanisms predisposing individuals to an increased risk for development of hypertension.—Pinto, V., Pinho, M. J., Soares-da-Silva, P. Renal amino acid transport systems and essential hypertension.
机译:几项临床和动物研究表明,“血压随着肾脏,”,即肾脏的肾脏转基因的肾脏受到高血压的正常受体将产生高血压。 Intrarenal多巴胺通过调节上皮钠运输,在高血压发病中起着重要作用。 L-DOPA的候选传送系统,多巴胺的源,包括钠依赖性系统B0,B0,+和Y + L,以及独立于钠的系统L(LAT1和LAT2)和B0,+。肾LAT2在预血压性自发性高血压大鼠(SHR)中过表达,这可能有助于增强近端小管的L-DOPA摄取和增加多巴胺产生,因为克服D1受体功能的缺陷。另一方面,它最近据报道,精氨酸转运受损有助于在ShR肾髓质中观察到的低肾脏一氧化氮生物利用度。在这里,我们审查了肾脏氨基酸转运蛋白在肾脏中的重要性,并突出了这些转运蛋白在原发性高血压中表达和调节的病理生理变化。对肾氨基酸转运蛋白的调节的研究可能有助于将介绍性质的潜在机制定义为高血压的发育风险增加。 - Pinto,V.,Pinho,MJ,Soares-Da-Silva,P.肾氨基酸输送系统和必需的高血压。

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