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

Sophie de Seigneux, Hans Malte, Henrik Dimke, Jørgen Frøkiaer, Søren Nielsen, Sebastian Frische

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Resumé

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
OriginalsprogEngelsk
TidsskriftAmerican Journal of Physiology: Renal Physiology
Vol/bind292
Udgave nummer4
Sider (fra-til)F1256-66
ISSN1931-857X
DOI
StatusUdgivet - apr. 2007
Udgivet eksterntJa

Fingeraftryk

Respiratory Acidosis
Hypercapnia
Down-Regulation
Kidney
Wistar Rats

Citer dette

de Seigneux, Sophie ; Malte, Hans ; Dimke, Henrik ; Frøkiaer, Jørgen ; Nielsen, Søren ; Frische, Sebastian. / Renal compensation to chronic hypoxic hypercapnia : downregulation of pendrin and adaptation of the proximal tubule. I: American Journal of Physiology: Renal Physiology. 2007 ; Bind 292, Nr. 4. s. F1256-66.
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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",
keywords = "Acidosis, Respiratory, Adaptation, Physiological, Animals, Anoxia, Aquaporin 2, Calbindins, Carbon Dioxide, Chloride-Bicarbonate Antiporters, Chlorides, Down-Regulation, Epithelial Sodium Channels, Hydrogen-Ion Concentration, Hypercapnia, Immunohistochemistry, Kidney, Kidney Tubules, Proximal, Male, Oxygen, Partial Pressure, Rats, S100 Calcium Binding Protein G, Sodium-Bicarbonate Symporters, Sodium-Hydrogen Antiporter, Vacuolar Proton-Translocating ATPases",
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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.

I: American Journal of Physiology: Renal Physiology, Bind 292, Nr. 4, 04.2007, s. F1256-66.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

TY - JOUR

T1 - Renal compensation to chronic hypoxic hypercapnia

T2 - 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

PY - 2007/4

Y1 - 2007/4

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

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

KW - Acidosis, Respiratory

KW - Adaptation, Physiological

KW - Animals

KW - Anoxia

KW - Aquaporin 2

KW - Calbindins

KW - Carbon Dioxide

KW - Chloride-Bicarbonate Antiporters

KW - Chlorides

KW - Down-Regulation

KW - Epithelial Sodium Channels

KW - Hydrogen-Ion Concentration

KW - Hypercapnia

KW - Immunohistochemistry

KW - Kidney

KW - Kidney Tubules, Proximal

KW - Male

KW - Oxygen

KW - Partial Pressure

KW - Rats

KW - S100 Calcium Binding Protein G

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 -