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[遗传源性动脉高血压中的钠转运与肾血流动力学:原发性还是继发性改变?]

[Sodium transport and renal hemodynamics in arterial hypertension of genetic origin: primary or secondary changes?].

作者信息

Barlassina C, Cusi D, Pati P, Ferrari P, Salardi S, Bianchi G

机构信息

Istituto di Scienze Mediche, Scuola di Specializzazione in Nefrologia Medica, Universitá di Milano.

出版信息

Nephrologie. 1988;9(1):9-13.

PMID:3292964
Abstract

Essential hypertension develops from the interaction of genetic and environmental factors. In the Milan hypertensive strain (MHS) rat before the development of hypertension, there is a genetically inherited increase of tubular reabsorption which is the cause of the following increase of blood pressure. Also in young normotensive humans, predisposed to develop essential hypertension later in life, there is an abnormal pattern of renal function that may be explained by increase of tubular reabsorption. The studies of the erythrocyte membrane transport support these data and suggest that at least a subset of essential hypertensive humans may develop a form of hypertension that has pathogenetic mechanisms similar to the ones of MHS rats.

摘要

原发性高血压由遗传和环境因素相互作用所致。在米兰高血压大鼠品系(MHS)发生高血压之前,存在遗传性肾小管重吸收增加,这是随后血压升高的原因。同样,在日后易患原发性高血压的年轻血压正常人群中,也存在肾功能异常模式,这可能是由肾小管重吸收增加所解释的。红细胞膜转运研究支持了这些数据,并表明至少一部分原发性高血压患者可能发展出一种具有与MHS大鼠相似发病机制的高血压形式。

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