结肠H⁺-K⁺-ATP酶在钾缺乏时被诱导，并介导内髓集合管中HCO₃⁻重吸收增加。

Colonic H+-K+-ATPase is induced and mediates increased HCO3- reabsorption in inner medullary collecting duct in potassium depletion.

作者信息

Nakamura S, Amlal H, Galla J H, Soleimani M

机构信息

Department of Medicine, University of Cincinnati School of Medicine, and Veterans Affairs Medical Center, Ohio, USA.

出版信息

Kidney Int. 1998 Oct;54(4):1233-9. doi: 10.1046/j.1523-1755.1998.00105.x.

DOI:10.1046/j.1523-1755.1998.00105.x

PMID:9767539

Abstract

BACKGROUND

Potassium depletion increases HCO3- reabsorption in outer medullary collecting duct (OMCD) by activation of colonic (c) H-K-ATPase (HKA). The purpose of the current experiments was to examine the role of the isoforms of HKA in HCO3- reabsorption by terminal inner medullary collecting duct (IMCD) cells in potassium depletion.

METHODS

Sprague-Dawley rats were fed a potassium-free diet and studied after 8 to 10 days. mRNA expression of HKA isoforms in terminal portion of inner medulla was examined and correlated with HCO3- reabsorption in the terminal IMCD.

RESULTS

Gastric (g) HKA mRNA decreased whereas colonic (c) HKA mRNA expression was heavily induced in terminal portion of inner medulla in potassium depleted rats. Net HCO3- flux (JtCO2) in terminal IMCD increased in potassium depletion (4.56 to 7.06 pmol/min/mm tubule length, P < 0.001). In normal rats, 1 mM ouabain in perfusate had no effect on JtCO2, whereas 10 microM Schering 28080 (SCH) decreased JtCO2 to 2.4 (P < 0.002). In KD rats, 1 mM ouabain decreased JtCO2 to 4.9 (P < 0.005) and 10 microM SCH decreased JtCO2 to 3.3 (P < 0.001). However, the inhibitory effects of SCH and ouabain on JtCO2 in potassium depleted animals were not additive.

CONCLUSIONS

The data indicate that gHKA is suppressed whereas cHKA is induced in potassium depletion and mediates increased HCO3- reabsorption in terminal IMCD. The results further indicate that cHKA in vivo is sensitive to both SCH and ouabain.

摘要

背景

钾缺乏通过激活结肠型（c）H-K-ATP酶（HKA）增加外髓集合管（OMCD）中HCO3-的重吸收。本实验的目的是研究HKA同工型在钾缺乏时终末内髓集合管（IMCD）细胞HCO3-重吸收中的作用。

方法

给Sprague-Dawley大鼠喂食无钾饮食，8至10天后进行研究。检测内髓终末部分HKA同工型的mRNA表达，并与终末IMCD中HCO3-的重吸收进行相关性分析。

结果

在钾缺乏的大鼠中，胃型（g）HKA mRNA减少，而结肠型（c）HKA mRNA表达在内髓终末部分被显著诱导。钾缺乏时终末IMCD中的净HCO3-通量（JtCO2）增加（从4.56增加至7.06 pmol/分钟/毫米肾小管长度，P < 0.001）。在正常大鼠中，灌注液中1 mM哇巴因对JtCO2无影响，而10 μM先灵28080（SCH）使JtCO2降至2.4（P < 0.002）。在钾缺乏大鼠中，1 mM哇巴因使JtCO2降至4.9（P < 0.005），10 μM SCH使JtCO2降至3.3（P < 0.001）。然而，SCH和哇巴因对钾缺乏动物JtCO2的抑制作用并非相加的。