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基础研究:远端肾小管性酸中毒中的失盐现象——新视角,老问题。

Basic research: Salt wasting in distal renal tubular acidosis-new look, old problem.

机构信息

Departments of Medicine and Physiology, and Cellular Biophysics, College of Physicians & Surgeons of Columbia University, 630 West 168th Street, New York, NY 10032, USA.

出版信息

Nat Rev Nephrol. 2013 Dec;9(12):712-3. doi: 10.1038/nrneph.2013.235. Epub 2013 Nov 5.

Abstract

Acidosis affects sodium and potassium excretion, likely via the pH sensitivity of ion transporters. A recent paper shows that β-intercalated cells with deleted H(+)-ATPase release ATP into urine, which induces the production of prostaglandin E2 (PGE2). PGE2 then reduces sodium absorption in the principal cells of the cortical collecting tubule and increases potassium secretion.

摘要

酸中毒会影响钠和钾的排泄,这可能是通过离子转运体对 pH 值的敏感性实现的。最近的一篇论文表明,缺乏 H(+)-ATPase 的β插入细胞会将 ATP 释放到尿液中,这会诱导前列腺素 E2(PGE2)的产生。PGE2 随后减少皮质集合管主细胞对钠的吸收,并增加钾的分泌。

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