Kleinman J G
Medical College of Wisconsin, Section of Nephrology, Milwaukee.
J Am Soc Nephrol. 1994 Nov;5(5 Suppl 1):S6-11. doi: 10.1681/ASN.V55s6.
Acidification of the urine is mediated by vectorial H+ transport from cells at a number of sites in the kidney. A proton ATPase has been described that appears to mediate a significant proportion of this H+ transport. In particular, in proximal tubule and collecting duct, there is evidence both for the presence of transporter protein and for H+ transport with features that have been identified with it. This review highlights some of the unresolved questions regarding this transporter, specifically, its distribution and relationship to the vacuolar pump present in endocytotic vesicles, how physiologic control is asserted, and its role in pathophysiology. The review discusses in greater detail the issue of whether the vacuolar H+ ATPase is responsible for all of the urinary acidification and concludes that it probably is not. Specifically, compelling evidence for acidification at sites in the kidney that appear to lack this transporter is presented. In addition, the evidence for the presence in the kidney of a gastric-type H(+)-K+ ATPase is also reviewed. The evidence appears to be strong for a K(+)-stimulated ATPase that is sensitive to omeprazole and SCH 28080, the prototypical H(+)-K+ ATPase inhibitors; however, uncertainties remain because of problems of transport inhibition specificity and discordant results of molecular biologic studies.
尿液酸化是由肾脏多个部位的细胞进行矢量性氢离子转运介导的。已经描述了一种质子ATP酶，它似乎介导了很大一部分这种氢离子转运。特别是在近端小管和集合管中，有证据表明存在转运蛋白以及具有与其相关特征的氢离子转运。本综述强调了关于这种转运蛋白的一些未解决问题，具体而言，其分布以及与内吞小泡中存在的液泡泵的关系、生理控制是如何施加的，以及它在病理生理学中的作用。该综述更详细地讨论了液泡氢离子ATP酶是否负责所有尿液酸化这一问题，并得出结论认为可能并非如此。具体而言，文中展示了在肾脏中似乎缺乏这种转运蛋白的部位存在酸化的有力证据。此外，还综述了肾脏中存在胃型氢离子 - 钾离子ATP酶的证据。对于一种对奥美拉唑和SCH 28080（典型的氢离子 - 钾离子ATP酶抑制剂）敏感的钾离子刺激的ATP酶，证据似乎很充分；然而，由于转运抑制特异性问题和分子生物学研究结果不一致，仍存在不确定性。
