Jørgen Frøkiær

Renal compensation to chronic hypoxic hypercapnia: downregulation of pendrin and adaptation of the proximal tubule

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Renal compensation to chronic hypoxic hypercapnia: downregulation of pendrin and adaptation of the proximal tubule. / de Seigneux, Sophie; Malte, Hans; Dimke, Henrik; Frøkiaer, Jørgen; Nielsen, Søren; Frische, Sebastian; Dimke, Henrik Anthony.

In: American Journal of Physiology: Renal Physiology, Vol. 292, No. 4, 2007, p. F1256-66.

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

Harvard

de Seigneux, S, Malte, H, Dimke, H, Frøkiaer, J, Nielsen, S, Frische, S & Dimke, HA 2007, 'Renal compensation to chronic hypoxic hypercapnia: downregulation of pendrin and adaptation of the proximal tubule', American Journal of Physiology: Renal Physiology, vol. 292, no. 4, pp. F1256-66. https://doi.org/10.1152/ajprenal.00220.2006

APA

de Seigneux, S., Malte, H., Dimke, H., Frøkiaer, J., Nielsen, S., Frische, S., & Dimke, H. A. (2007). Renal compensation to chronic hypoxic hypercapnia: downregulation of pendrin and adaptation of the proximal tubule. American Journal of Physiology: Renal Physiology, 292(4), F1256-66. https://doi.org/10.1152/ajprenal.00220.2006

CBE

de Seigneux S, Malte H, Dimke H, Frøkiaer J, Nielsen S, Frische S, Dimke HA. 2007. Renal compensation to chronic hypoxic hypercapnia: downregulation of pendrin and adaptation of the proximal tubule. American Journal of Physiology: Renal Physiology. 292(4):F1256-66. https://doi.org/10.1152/ajprenal.00220.2006

MLA

Vancouver

de Seigneux S, Malte H, Dimke H, Frøkiaer J, Nielsen S, Frische S et al. Renal compensation to chronic hypoxic hypercapnia: downregulation of pendrin and adaptation of the proximal tubule. American Journal of Physiology: Renal Physiology. 2007;292(4):F1256-66. https://doi.org/10.1152/ajprenal.00220.2006

Author

de Seigneux, Sophie ; Malte, Hans ; Dimke, Henrik ; Frøkiaer, Jørgen ; Nielsen, Søren ; Frische, Sebastian ; Dimke, Henrik Anthony. / Renal compensation to chronic hypoxic hypercapnia: downregulation of pendrin and adaptation of the proximal tubule. In: American Journal of Physiology: Renal Physiology. 2007 ; Vol. 292, No. 4. pp. F1256-66.

Bibtex

@article{796150016c82499e8f3afbb49189e437,
title = "Renal compensation to chronic hypoxic hypercapnia: downregulation of pendrin and adaptation of the proximal tubule",
abstract = "The molecular basis for the renal compensation to respiratory acidosis and specifically the role of pendrin in this condition are unclear. Therefore, we studied the adaptation of the proximal tubule and the collecting duct to respiratory acidosis. Male Wistar-Hannover rats were exposed to either hypercapnia and hypoxia [8% CO(2) and 13% O(2) (hypercapnic, n = 6) or normal air (controls, n = 6)] in an environmental chamber for 10 days and were killed under the same atmosphere. In hypercapnic rats, arterial pH was lower than controls (7.31 +/- 0.01 vs. 7.39 +/- 0.01, P = 0.03), blood HCO(3)(-) concentration was increased (42 +/- 0.9 vs. 32 +/- 0.24 mM, P <0.001), arterial Pco(2) was increased (10.76 +/- 0.4 vs. 7.20 +/- 0.4 kPa, P <0.001), and plasma chloride concentration was decreased (92.2 +/- 0.7 vs. 97.2 +/- 0.5 mM, P <0.001). Plasma aldosterone levels were unchanged. In the proximal tubule, immunoblotting showed an increased expression of sodium/bicarbonate exchanger protein (188 +/- 22 vs. 100 +/- 11%, P = 0.005), confirmed by immunohistochemistry. Total Na/H exchanger protein expression in the cortex was unchanged by immunoblotting (119 +/- 10 vs. 100 +/- 11%, P = 0.27) and immunohistochemistry. In the cortex, the abundance of pendrin was decreased (51 +/- 9 vs. 100 +/- 7%, P = 0.003) by immunoblotting. Immunohistochemistry revealed that this decrease was clear in both cortical collecting ducts (CCDs) and connecting tubules (CNTs). This demonstrates that pendrin expression can be regulated in acidotic animals with no changes in aldosterone levels and no external chloride load. This reduction of pendrin expression may help in redirecting the CNT and CCD toward chloride excretion and bicarbonate reabsorption, contributing to the increased plasma bicarbonate and decreased plasma chloride of chronic respiratory acidosis.",
keywords = "Acidosis, Respiratory, Adaptation, Physiological, Animals, Anoxia, Aquaporin 2, Calcium-Binding Protein, Vitamin D-Dependent, Carbon Dioxide, Chloride-Bicarbonate Antiporters, Chlorides, Down-Regulation, Epithelial Sodium Channel, Hydrogen-Ion Concentration, Hypercapnia, Immunohistochemistry, Kidney, Kidney Tubules, Proximal, Male, Oxygen, Partial Pressure, Rats, Sodium-Bicarbonate Symporters, Sodium-Hydrogen Antiporter, Vacuolar Proton-Translocating ATPases",
author = "{de Seigneux}, Sophie and Hans Malte and Henrik Dimke and J{\o}rgen Fr{\o}kiaer and S{\o}ren Nielsen and Sebastian Frische and Dimke, {Henrik Anthony}",
year = "2007",
doi = "10.1152/ajprenal.00220.2006",
language = "English",
volume = "292",
pages = "F1256--66",
journal = "American Journal of Physiology: Renal Physiology",
issn = "1931-857X",
publisher = "American Physiological Society",
number = "4",

}

RIS

TY - JOUR

T1 - Renal compensation to chronic hypoxic hypercapnia: downregulation of pendrin and adaptation of the proximal tubule

AU - de Seigneux, Sophie

AU - Malte, Hans

AU - Dimke, Henrik

AU - Frøkiaer, Jørgen

AU - Nielsen, Søren

AU - Frische, Sebastian

AU - Dimke, Henrik Anthony

PY - 2007

Y1 - 2007

N2 - The molecular basis for the renal compensation to respiratory acidosis and specifically the role of pendrin in this condition are unclear. Therefore, we studied the adaptation of the proximal tubule and the collecting duct to respiratory acidosis. Male Wistar-Hannover rats were exposed to either hypercapnia and hypoxia [8% CO(2) and 13% O(2) (hypercapnic, n = 6) or normal air (controls, n = 6)] in an environmental chamber for 10 days and were killed under the same atmosphere. In hypercapnic rats, arterial pH was lower than controls (7.31 +/- 0.01 vs. 7.39 +/- 0.01, P = 0.03), blood HCO(3)(-) concentration was increased (42 +/- 0.9 vs. 32 +/- 0.24 mM, P <0.001), arterial Pco(2) was increased (10.76 +/- 0.4 vs. 7.20 +/- 0.4 kPa, P <0.001), and plasma chloride concentration was decreased (92.2 +/- 0.7 vs. 97.2 +/- 0.5 mM, P <0.001). Plasma aldosterone levels were unchanged. In the proximal tubule, immunoblotting showed an increased expression of sodium/bicarbonate exchanger protein (188 +/- 22 vs. 100 +/- 11%, P = 0.005), confirmed by immunohistochemistry. Total Na/H exchanger protein expression in the cortex was unchanged by immunoblotting (119 +/- 10 vs. 100 +/- 11%, P = 0.27) and immunohistochemistry. In the cortex, the abundance of pendrin was decreased (51 +/- 9 vs. 100 +/- 7%, P = 0.003) by immunoblotting. Immunohistochemistry revealed that this decrease was clear in both cortical collecting ducts (CCDs) and connecting tubules (CNTs). This demonstrates that pendrin expression can be regulated in acidotic animals with no changes in aldosterone levels and no external chloride load. This reduction of pendrin expression may help in redirecting the CNT and CCD toward chloride excretion and bicarbonate reabsorption, contributing to the increased plasma bicarbonate and decreased plasma chloride of chronic respiratory acidosis.

AB - The molecular basis for the renal compensation to respiratory acidosis and specifically the role of pendrin in this condition are unclear. Therefore, we studied the adaptation of the proximal tubule and the collecting duct to respiratory acidosis. Male Wistar-Hannover rats were exposed to either hypercapnia and hypoxia [8% CO(2) and 13% O(2) (hypercapnic, n = 6) or normal air (controls, n = 6)] in an environmental chamber for 10 days and were killed under the same atmosphere. In hypercapnic rats, arterial pH was lower than controls (7.31 +/- 0.01 vs. 7.39 +/- 0.01, P = 0.03), blood HCO(3)(-) concentration was increased (42 +/- 0.9 vs. 32 +/- 0.24 mM, P <0.001), arterial Pco(2) was increased (10.76 +/- 0.4 vs. 7.20 +/- 0.4 kPa, P <0.001), and plasma chloride concentration was decreased (92.2 +/- 0.7 vs. 97.2 +/- 0.5 mM, P <0.001). Plasma aldosterone levels were unchanged. In the proximal tubule, immunoblotting showed an increased expression of sodium/bicarbonate exchanger protein (188 +/- 22 vs. 100 +/- 11%, P = 0.005), confirmed by immunohistochemistry. Total Na/H exchanger protein expression in the cortex was unchanged by immunoblotting (119 +/- 10 vs. 100 +/- 11%, P = 0.27) and immunohistochemistry. In the cortex, the abundance of pendrin was decreased (51 +/- 9 vs. 100 +/- 7%, P = 0.003) by immunoblotting. Immunohistochemistry revealed that this decrease was clear in both cortical collecting ducts (CCDs) and connecting tubules (CNTs). This demonstrates that pendrin expression can be regulated in acidotic animals with no changes in aldosterone levels and no external chloride load. This reduction of pendrin expression may help in redirecting the CNT and CCD toward chloride excretion and bicarbonate reabsorption, contributing to the increased plasma bicarbonate and decreased plasma chloride of chronic respiratory acidosis.

KW - Acidosis, Respiratory

KW - Adaptation, Physiological

KW - Animals

KW - Anoxia

KW - Aquaporin 2

KW - Calcium-Binding Protein, Vitamin D-Dependent

KW - Carbon Dioxide

KW - Chloride-Bicarbonate Antiporters

KW - Chlorides

KW - Down-Regulation

KW - Epithelial Sodium Channel

KW - Hydrogen-Ion Concentration

KW - Hypercapnia

KW - Immunohistochemistry

KW - Kidney

KW - Kidney Tubules, Proximal

KW - Male

KW - Oxygen

KW - Partial Pressure

KW - Rats

KW - Sodium-Bicarbonate Symporters

KW - Sodium-Hydrogen Antiporter

KW - Vacuolar Proton-Translocating ATPases

U2 - 10.1152/ajprenal.00220.2006

DO - 10.1152/ajprenal.00220.2006

M3 - Journal article

C2 - 17182533

VL - 292

SP - F1256-66

JO - American Journal of Physiology: Renal Physiology

JF - American Journal of Physiology: Renal Physiology

SN - 1931-857X

IS - 4

ER -