Pendrin in the mouse kidney is primarily regulated by Cl- excretion but also by systemic metabolic acidosis

被引:46
|
作者
Hafner, Patricia [1 ,2 ]
Grimaldi, Rosa [1 ,2 ,3 ]
Capuano, Paola [1 ,2 ]
Capasso, Giovambattista [3 ]
Wagner, Carsten A. [1 ,2 ]
机构
[1] Univ Zurich, Inst Physiol, CH-8057 Zurich, Switzerland
[2] Univ Zurich, Ctr Human Integrat Physiol, CH-8057 Zurich, Switzerland
[3] Univ Naples 2, Sch Med, Naples, Italy
来源
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY | 2008年 / 295卷 / 06期
基金
新加坡国家研究基金会;
关键词
transporter; collecting duct;
D O I
10.1152/ajpcell.00419.2008
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Hafner P, Grimaldi R, Capuano P, Capasso G, Wagner CA. Pendrin in the mouse kidney is primarily regulated by Cl- excretion but also by systemic metabolic acidosis. Am J Physiol Cell Physiol 295: C1658-C1667, 2008; doi:10.1152/ajpcell.00419.2008.-The Cl-/anion exchanger pendrin (SLC26A4) is expressed on the apical side of renal non-type A intercalated cells. The abundance of pendrin is reduced during metabolic acidosis induced by oral NH4Cl loading. More recently, it has been shown that pendrin expression is increased during conditions associated with decreased urinary Cl- excretion and decreased upon Cl- loading. Hence, it is unclear if pendrin regulation during NH4Cl-induced acidosis is primarily due the Cl- load or acidosis. Therefore, we treated mice to increase urinary acidification, induce metabolic acidosis, or provide an oral Cl- load and examined the systemic acid-base status, urinary acidification, urinary Cl- excretion, and pendrin abundance in the kidney. NaCl or NH4Cl increased urinary Cl- excretion, whereas (NH4)(2)SO4, Na2SO4, and acetazolamide treatments decreased urinary Cl- excretion. NH4Cl, (NH4)(2)SO4, and acetazolamide caused metabolic acidosis and stimulated urinary net acid excretion. Pendrin expression was reduced under NaCl, NH4Cl, and (NH4)(2)SO4 loading and increased with the other treatments. (NH4)(2)SO4 and acetazolamide treatments reduced the relative number of pendrin-expressing cells in the collecting duct. In a second series, animals were kept for 1 and 2 wk on a low-protein (20%) diet or a high-protein (50%) diet. The high-protein diet slightly increased urinary Cl- excretion and strongly stimulated net acid excretion but did not alter pendrin expression. Thus, pendrin expression is primarily correlated with urinary Cl- excretion but not blood Cl-. However, metabolic acidosis caused by acetazolamide or (NH4)(2)SO4 loading prevented the increase or even reduced pendrin expression despite low urinary Cl- excretion, suggesting an independent regulation by acid-base status.
引用
收藏
页码:C1658 / C1667
页数:10
相关论文
共 41 条
  • [31] URINARY-EXCRETION OF N-ACETYL-BETA-D-GLUCOSAMINIDASE IN CHILDREN WITH NH4CL METABOLIC-ACIDOSIS
    GUIGNARD, JP
    SULYOK, E
    GYORKE, Z
    ACTA PAEDIATRICA SCANDINAVICA, 1990, 79 (11): : 1116 - 1117
  • [32] Transmembrane Protein 16A (TMEM16A) Is a Ca2+-regulated Cl- Secretory Channel in Mouse Airways
    Rock, Jason R.
    O'Neal, Wanda K.
    Gabriel, Sherif E.
    Randell, Scott H.
    Harfe, Brian D.
    Boucher, Richard C.
    Grubb, Barbara R.
    JOURNAL OF BIOLOGICAL CHEMISTRY, 2009, 284 (22) : 14875 - 14880
  • [33] Astrocytes from mouse brain slices express ClC-2-mediated Cl- currents regulated during development and after injury
    Makara, JK
    Rappert, A
    Matthias, K
    Steinhäuser, C
    Spät, A
    Kettenmann, H
    MOLECULAR AND CELLULAR NEUROSCIENCE, 2003, 23 (04) : 521 - 530
  • [34] Upregulation of the secretory-type Na+/K+C/2Cl+-cotransporter in the kidney by metabolic acidosis and dehydration in rats
    Ikebe, M
    Nonoguchi, H
    Nakayama, Y
    Tashima, Y
    Tomita, K
    JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 2001, 12 (03): : 423 - 430
  • [35] Contribution of Na+, HCO3-/Cl- exchanger activity on recovery from induced-acidosis in oocyte, zygote and embryo of Balb/c strain mouse.
    Erdogan, Seref
    Cetinkaya, Ali
    Dogan, Ayse
    BIOLOGY OF REPRODUCTION, 2007, : 92 - 92
  • [36] Mouse down-regulated in adenoma (DRA) is an intestinal Cl-/HCO3- exchanger and is up-regulated in colon of mice lacking the NHE3 Na+/H+ exchanger
    Melvin, JE
    Park, K
    Richardson, L
    Schultheis, PJ
    Shull, GE
    JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (32) : 22855 - 22861
  • [37] HCO3-/Cl- Exchange Inactivation and Reactivation during Mouse Oocyte Meiosis Correlates with MEK/MAPK-Regulated Ae2 Plasma Membrane Localization
    Zhou, Chenxi
    Tiberi, Mario
    Liang, Binhui
    Alper, Seth L.
    Baltz, Jay M.
    PLOS ONE, 2009, 4 (10):
  • [38] EFFECTS OF GLUCAGON ON NA+, CL-, K+, MG-2+ AND CA-2+ TRANSPORTS IN CORTICAL AND MEDULLARY THICK ASCENDING LIMBS OF MOUSE KIDNEY
    DISTEFANO, A
    WITTNER, M
    NITSCHKE, R
    BRAITSCH, R
    GREGER, R
    BAILLY, C
    AMIEL, C
    ELALOUF, JM
    ROINEL, N
    DEROUFFIGNAC, C
    PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY, 1989, 414 (06): : 640 - 646
  • [39] Extracellular pH alkalinization by Cl-/HCO3- exchanger is crucial for TASK2 activation by hypotonic shock in proximal cell lines from mouse kidney
    L'Hoste, S.
    Barriere, H.
    Belfodil, R.
    Rubera, I.
    Duranton, C.
    Tauc, M.
    Poujeol, C.
    Barhanin, J.
    Poujeol, P.
    AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, 2007, 292 (02) : F628 - F638
  • [40] Potassium restriction, high protein intake, and metabolic acidosis increase expression of the glutamine transporter SNAT3 (Slc38a3) in mouse kidney
    Busque, Stephanie M.
    Wagner, Carsten A.
    AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, 2009, 297 (02) : F440 - F450