钾离子缺乏通过激活结肠氢离子-钾离子-ATP酶增加外髓集合管中碳酸氢根离子的重吸收。

K+ depletion increases HCO3- reabsorption in OMCD by activation of colonic H(+)-K(+)-ATPase.

作者信息

Nakamura S, Wang Z, Galla J H, Soleimani M

机构信息

Department of Medicine, University of Cincinnati School of Medicine, Ohio, USA.

出版信息

Am J Physiol. 1998 Apr;274(4):F687-92. doi: 10.1152/ajprenal.1998.274.4.F687.

DOI:10.1152/ajprenal.1998.274.4.F687

PMID:9575892

Abstract

To probe the role of the isoforms of H(+)-K(+)-ATPase (HKA) in potassium depletion (KD), rats were placed on a KD diet for 2 wk. Colonic HKA (cHKA) mRNA levels increased approximately 30-fold in outer medulla, and net HCO3-flux (JtCO2) in outer medullary collecting duct (OMCD) increased (13.1 pmol.min-1.mm tubule length-1 in control to 17.7 pmol.min-1.mm tubule length-1 in KD; P < 0.01). In normal rats, 1 mM ouabain in perfusate had no effect on JtCO2, whereas 10 microM Sch-28080 decreased JtCO2 to 5.1 pmol.min-1.mm tubule length-1 (P < 0.001). In KD rats, ouabain 1 mM decreased JtCO2 to 6.3 pmol.min-1.mm tubule length-1 (P < 0.001). Although 10 microM Sch-28080 also decreased JtCO2 to 4.6 pmol.min-1.mm tubule length-1 (P < 0.001), the inhibitory effects of Sch-28080 and ouabain were not additive. Removal of K+ from perfusate blocked Sch-28080-sensitive JtCO2 in both normal and KD tubules. The data suggest that, in KD, cHKA is induced and mediates increased HCO3-reabsorption in OMCD, cHKA in vivo is sensitive to both Sch-28080 and ouabain, and cHKA activity is dominant.

摘要

为探究H⁺-K⁺-ATP酶（HKA）同工型在钾缺乏（KD）中的作用，将大鼠置于低钾饮食2周。结肠HKA（cHKA）mRNA水平在外髓质中增加约30倍，外髓质集合管（OMCD）中的净HCO₃通量（JtCO₂）增加（对照组为13.1 pmol·min⁻¹·mm肾小管长度⁻¹，低钾组为17.7 pmol·min⁻¹·mm肾小管长度⁻¹；P<0.01）。在正常大鼠中，灌注液中1 mM哇巴因对JtCO₂无影响，而10 μM Sch-28080可使JtCO₂降至5.1 pmol·min⁻¹·mm肾小管长度⁻¹（P<0.001）。在低钾大鼠中，1 mM哇巴因可使JtCO₂降至6.3 pmol·min⁻¹·mm肾小管长度⁻¹（P<0.001）。尽管10 μM Sch-28080也可使JtCO₂降至4.6 pmol·min⁻¹·mm肾小管长度⁻¹（P<0.001），但Sch-28080和哇巴因的抑制作用无相加性。从灌注液中去除K⁺可阻断正常和低钾肾小管中对Sch-28080敏感的JtCO₂。数据表明，在低钾状态下，cHKA被诱导并介导OMCD中HCO₃重吸收增加，体内cHKA对Sch-28080和哇巴因均敏感，且cHKA活性占主导。