钾缺乏刺激存活大鼠远端肾小管的体内重吸收。（注：原文中“HCO3”应改为“HCO₃”，完整准确的译文应该是：钾缺乏刺激存活大鼠远端肾小管的体内碳酸氢根重吸收。）

K depletion stimulates in vivo HCO3 reabsorption in surviving rat distal tubules.

作者信息

Levine D Z, Iacovitti M, Buckman S, Luck B, Hincke M T, Burns K D, Fryer J N

机构信息

Department of Medicine, University of Ottawa, Ontario, Canada.

出版信息

Am J Physiol. 1998 Apr;274(4):F665-72. doi: 10.1152/ajprenal.1998.274.4.F665.

DOI:10.1152/ajprenal.1998.274.4.F665

PMID:9575889

Abstract

To evaluate whether K depletion enhances in vivo bicarbonate reabsorption (JtCO2) in surviving distal tubules (DT), we compared DT JtCO2 in five-sixths nephrectomized rats (Nx) with and without dietary K depletion (Nx-K). Furthermore, to identify possible mechanisms of increased JtCO2, we perfused inhibitors of proton secretion in both Nx and Nx-K rats. JtCO2 (102 +/- 8 pmol.min-1.mm-1) was significantly increased in Nx-K vs. Nx rats (65 +/- 7 pmol.min-1.mm-1, P < 0.05) but unaffected by 10(-6) M losartan perfusion (94 +/- 6 pmol.min-1.mm-1, P = not significant). Although 10(-5) M Sch-28080 also had no significant effect, 5 x 10(-9) M concanamycin A perfusion significantly decreased JtCO2 in Nx-K rats to 65 +/- 8 pmol.min-1. mm-1 (P < 0.05). Morphometric evaluation and H(+)-ATPase immunogold labeling of Nx-K A-type intercalated cells revealed cellular hypertrophy, elaborated apical microplicae, and enhanced H(+)-ATPase apical polarization. Accordingly, these combined studies confirm that K depletion enhances JtCO2 in surviving DT by stimulating H(+)-ATPase activity, independent of the AT1 receptor.

摘要

为了评估钾缺乏是否会增强存活的远端肾小管（DT）中体内重碳酸盐的重吸收（JtCO2），我们比较了五分之六肾切除大鼠（Nx）在有或没有饮食性钾缺乏（Nx-K）情况下的DT JtCO2。此外，为了确定JtCO2增加的可能机制，我们在Nx和Nx-K大鼠中灌注了质子分泌抑制剂。与Nx大鼠（65±7 pmol·min-1·mm-1）相比，Nx-K大鼠的JtCO2（102±8 pmol·min-1·mm-1）显著增加（P<0.05），但不受10(-6) M氯沙坦灌注的影响（94±6 pmol·min-1·mm-1，P=无显著性差异）。虽然10(-5) M Sch-28080也没有显著影响，但5×10(-9) M concanamycin A灌注显著降低了Nx-K大鼠的JtCO2至65±8 pmol·min-1·mm-1（P<0.05）。对Nx-K A型闰细胞的形态计量学评估和H(+)-ATP酶免疫金标记显示细胞肥大、顶端微褶增多以及H(+)-ATP酶顶端极化增强。因此，这些联合研究证实，钾缺乏通过刺激H(+)-ATP酶活性增强了存活DT中的JtCO2，这一过程不依赖于AT1受体。