Jørgen Frøkiær

Altered expression of renal acid-base transporters in rats with lithium-induced NDI

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

Standard

Altered expression of renal acid-base transporters in rats with lithium-induced NDI. / Kim, Young-Hee; Kwon, Tae-Hwan; Christensen, Birgitte M et al.

In: American Journal of Physiology: Renal Physiology, Vol. 285, No. 6, 2003, p. F1244-57.

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

Harvard

Kim, Y-H, Kwon, T-H, Christensen, BM, Nielsen, J, Wall, SM, Madsen, KM, Frøkiaer, J & Nielsen, S 2003, 'Altered expression of renal acid-base transporters in rats with lithium-induced NDI', American Journal of Physiology: Renal Physiology, vol. 285, no. 6, pp. F1244-57. https://doi.org/10.1152/ajprenal.00176.2003

APA

Kim, Y-H., Kwon, T-H., Christensen, B. M., Nielsen, J., Wall, S. M., Madsen, K. M., Frøkiaer, J., & Nielsen, S. (2003). Altered expression of renal acid-base transporters in rats with lithium-induced NDI. American Journal of Physiology: Renal Physiology, 285(6), F1244-57. https://doi.org/10.1152/ajprenal.00176.2003

CBE

Kim Y-H, Kwon T-H, Christensen BM, Nielsen J, Wall SM, Madsen KM, Frøkiaer J, Nielsen S. 2003. Altered expression of renal acid-base transporters in rats with lithium-induced NDI. American Journal of Physiology: Renal Physiology. 285(6):F1244-57. https://doi.org/10.1152/ajprenal.00176.2003

MLA

Kim, Young-Hee et al. "Altered expression of renal acid-base transporters in rats with lithium-induced NDI". American Journal of Physiology: Renal Physiology. 2003, 285(6). F1244-57. https://doi.org/10.1152/ajprenal.00176.2003

Vancouver

Kim Y-H, Kwon T-H, Christensen BM, Nielsen J, Wall SM, Madsen KM et al. Altered expression of renal acid-base transporters in rats with lithium-induced NDI. American Journal of Physiology: Renal Physiology. 2003;285(6):F1244-57. https://doi.org/10.1152/ajprenal.00176.2003

Author

Kim, Young-Hee ; Kwon, Tae-Hwan ; Christensen, Birgitte M et al. / Altered expression of renal acid-base transporters in rats with lithium-induced NDI. In: American Journal of Physiology: Renal Physiology. 2003 ; Vol. 285, No. 6. pp. F1244-57.

Bibtex

@article{35fddeb0cc4611dd9710000ea68e967b,
title = "Altered expression of renal acid-base transporters in rats with lithium-induced NDI",
abstract = "Prolonged lithium treatment of humans and rodents often results in hyperchloremic metabolic acidosis. This is thought to be caused by diminished net H+ secretion and/or excessive back-diffusion of acid equivalents. To explore whether lithium treatment is associated with changes in the expression of key renal acid-base transporters, semiquantitative immunoblotting and immunocytochemistry were performed using kidneys from lithium-treated (n = 6) and control (n = 6) rats. Rats treated with lithium for 28 days showed decreased urine pH, whereas no significant differences in blood pH and plasma HCO3- levels were observed. Immunoblot analysis revealed that lithium treatment induced a significant increase in the expression of the H+-ATPase (B1-subunit) in cortex (190 +/- 18%) and inner stripe of the outer medulla (190 +/- 9%), and a dramatic increase in inner medulla (900 +/- 104%) in parallel to an increase in the expression of type 1 anion exchanger (400 +/- 40%). This was confirmed by immunocytochemistry and immunoelectron microscopy, which also revealed increased density of intercalated cells. Moreover, immunoblotting and immunocytochemistry revealed a significant increase in the expression of the type 1 electrogenic Na+-HCO3- cotransporter (NBC) in cortex (200 +/- 23%) and of the electroneutral NBCn1 in inner stripe of the outer medulla (250 +/- 54%). In contrast, there were no changes in the expression of Na+/H+ exchanger-3 or of the Cl-/HCO3- exchanger pendrin. These results demonstrate that the expression of specific renal acid-base transporters is markedly altered in response to long-term lithium treatment. This is likely to represent direct or compensatory effects to increase the capacity for HCO3- reabsorption, NH4+ reabsorption, and proton secretion to prevent the development of systemic metabolic acidosis.",
keywords = "Acidosis, Acids, Animals, Anion Exchange Protein 1, Erythrocyte, Antibody Specificity, Blotting, Western, Carrier Proteins, Diabetes Insipidus, Nephrogenic, Hydrogen-Ion Concentration, Immunohistochemistry, Kidney Cortex, Kidney Tubules, Collecting, Lithium, Male, Membrane Transport Proteins, Proton-Translocating ATPases, Rats, Rats, Sprague-Dawley, Sodium-Bicarbonate Symporters, Sodium-Hydrogen Antiporter, Urine",
author = "Young-Hee Kim and Tae-Hwan Kwon and Christensen, {Birgitte M} and Jakob Nielsen and Wall, {Susan M} and Madsen, {Kirsten M} and J{\o}rgen Fr{\o}kiaer and S{\o}ren Nielsen",
year = "2003",
doi = "10.1152/ajprenal.00176.2003",
language = "English",
volume = "285",
pages = "F1244--57",
journal = "American Journal of Physiology: Renal Physiology",
issn = "1931-857X",
publisher = "American Physiological Society",
number = "6",

}

RIS

TY - JOUR

T1 - Altered expression of renal acid-base transporters in rats with lithium-induced NDI

AU - Kim, Young-Hee

AU - Kwon, Tae-Hwan

AU - Christensen, Birgitte M

AU - Nielsen, Jakob

AU - Wall, Susan M

AU - Madsen, Kirsten M

AU - Frøkiaer, Jørgen

AU - Nielsen, Søren

PY - 2003

Y1 - 2003

N2 - Prolonged lithium treatment of humans and rodents often results in hyperchloremic metabolic acidosis. This is thought to be caused by diminished net H+ secretion and/or excessive back-diffusion of acid equivalents. To explore whether lithium treatment is associated with changes in the expression of key renal acid-base transporters, semiquantitative immunoblotting and immunocytochemistry were performed using kidneys from lithium-treated (n = 6) and control (n = 6) rats. Rats treated with lithium for 28 days showed decreased urine pH, whereas no significant differences in blood pH and plasma HCO3- levels were observed. Immunoblot analysis revealed that lithium treatment induced a significant increase in the expression of the H+-ATPase (B1-subunit) in cortex (190 +/- 18%) and inner stripe of the outer medulla (190 +/- 9%), and a dramatic increase in inner medulla (900 +/- 104%) in parallel to an increase in the expression of type 1 anion exchanger (400 +/- 40%). This was confirmed by immunocytochemistry and immunoelectron microscopy, which also revealed increased density of intercalated cells. Moreover, immunoblotting and immunocytochemistry revealed a significant increase in the expression of the type 1 electrogenic Na+-HCO3- cotransporter (NBC) in cortex (200 +/- 23%) and of the electroneutral NBCn1 in inner stripe of the outer medulla (250 +/- 54%). In contrast, there were no changes in the expression of Na+/H+ exchanger-3 or of the Cl-/HCO3- exchanger pendrin. These results demonstrate that the expression of specific renal acid-base transporters is markedly altered in response to long-term lithium treatment. This is likely to represent direct or compensatory effects to increase the capacity for HCO3- reabsorption, NH4+ reabsorption, and proton secretion to prevent the development of systemic metabolic acidosis.

AB - Prolonged lithium treatment of humans and rodents often results in hyperchloremic metabolic acidosis. This is thought to be caused by diminished net H+ secretion and/or excessive back-diffusion of acid equivalents. To explore whether lithium treatment is associated with changes in the expression of key renal acid-base transporters, semiquantitative immunoblotting and immunocytochemistry were performed using kidneys from lithium-treated (n = 6) and control (n = 6) rats. Rats treated with lithium for 28 days showed decreased urine pH, whereas no significant differences in blood pH and plasma HCO3- levels were observed. Immunoblot analysis revealed that lithium treatment induced a significant increase in the expression of the H+-ATPase (B1-subunit) in cortex (190 +/- 18%) and inner stripe of the outer medulla (190 +/- 9%), and a dramatic increase in inner medulla (900 +/- 104%) in parallel to an increase in the expression of type 1 anion exchanger (400 +/- 40%). This was confirmed by immunocytochemistry and immunoelectron microscopy, which also revealed increased density of intercalated cells. Moreover, immunoblotting and immunocytochemistry revealed a significant increase in the expression of the type 1 electrogenic Na+-HCO3- cotransporter (NBC) in cortex (200 +/- 23%) and of the electroneutral NBCn1 in inner stripe of the outer medulla (250 +/- 54%). In contrast, there were no changes in the expression of Na+/H+ exchanger-3 or of the Cl-/HCO3- exchanger pendrin. These results demonstrate that the expression of specific renal acid-base transporters is markedly altered in response to long-term lithium treatment. This is likely to represent direct or compensatory effects to increase the capacity for HCO3- reabsorption, NH4+ reabsorption, and proton secretion to prevent the development of systemic metabolic acidosis.

KW - Acidosis

KW - Acids

KW - Animals

KW - Anion Exchange Protein 1, Erythrocyte

KW - Antibody Specificity

KW - Blotting, Western

KW - Carrier Proteins

KW - Diabetes Insipidus, Nephrogenic

KW - Hydrogen-Ion Concentration

KW - Immunohistochemistry

KW - Kidney Cortex

KW - Kidney Tubules, Collecting

KW - Lithium

KW - Male

KW - Membrane Transport Proteins

KW - Proton-Translocating ATPases

KW - Rats

KW - Rats, Sprague-Dawley

KW - Sodium-Bicarbonate Symporters

KW - Sodium-Hydrogen Antiporter

KW - Urine

U2 - 10.1152/ajprenal.00176.2003

DO - 10.1152/ajprenal.00176.2003

M3 - Journal article

C2 - 12944321

VL - 285

SP - F1244-57

JO - American Journal of Physiology: Renal Physiology

JF - American Journal of Physiology: Renal Physiology

SN - 1931-857X

IS - 6

ER -