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Jørgen Frøkiær

Unilateral Ureteral Obstruction Alters Expression of Acid-Base Transporters in Rat Kidney

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Unilateral Ureteral Obstruction Alters Expression of Acid-Base Transporters in Rat Kidney. / Wang, Guixian; Ring, Troels; Li, Chunling; Kim, Soo Wan; Wen, Jianguo; Djurhuus, Jens Christian; Nielsen, Søren; Frøkiær, Jørgen.

In: Journal of Urology, Vol. 182, No. 6, 2009, p. 2964-73.

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

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Wang, G, Ring, T, Li, C, Kim, SW, Wen, J, Djurhuus, JC, Nielsen, S & Frøkiær, J 2009, 'Unilateral Ureteral Obstruction Alters Expression of Acid-Base Transporters in Rat Kidney', Journal of Urology, vol. 182, no. 6, pp. 2964-73. https://doi.org/10.1016/j.juro.2009.08.013

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Author

Wang, Guixian ; Ring, Troels ; Li, Chunling ; Kim, Soo Wan ; Wen, Jianguo ; Djurhuus, Jens Christian ; Nielsen, Søren ; Frøkiær, Jørgen. / Unilateral Ureteral Obstruction Alters Expression of Acid-Base Transporters in Rat Kidney. In: Journal of Urology. 2009 ; Vol. 182, No. 6. pp. 2964-73.

Bibtex

@article{bf0eba70c9e911dea30a000ea68e967b,
title = "Unilateral Ureteral Obstruction Alters Expression of Acid-Base Transporters in Rat Kidney",
abstract = "PURPOSE: Unilateral ureteral obstruction is a common clinical problem that is often associated with a urinary acidification defect caused by decreased net H(+) secretion and/or HCO(3)(-) reabsorption. To clarify the molecular mechanisms of these defects we examined expression levels of key acid-base transporters along the renal nephron segments and collecting duct. MATERIALS AND METHODS: Wistar rats (M{\o}llegard Breeding Centre, Eiby, Denmark) underwent 24-hour unilateral ureteral obstruction, unilateral ureteral obstruction release followed for 4 days or unilateral ureteral obstruction release followed for 4 days plus experimental acidosis induced by NH(4)Cl oral administration. After sacrifice kidneys were processed for immunoblotting and immunohistochemistry. RESULTS: Semiquantitative immunoblotting revealed that unilateral ureteral obstruction caused significant mean +/- SE down-regulation of type 3 Na(+)/H(+) exchanger to 53% +/- 9%, electrogenic Na(+)/HCO(3)(-) cotransporter to 60% +/- 9%, type 1 bumetanide sensitive Na(+)-K(+)(NH(4)(+)) -2Cl(-) cotransporter to 64% +/- 7%, electroneutral Na(+)/HCO(3)(-) cotransporter to 43% +/- 4% and anion exchanger (pendrin) to 53% +/- 10% in the obstructed kidney, which was confirmed by immunohistochemistry. After release of unilateral ureteral obstruction down-regulation of these transporters persisted together with marked down-regulation of H(+)-adenosine triphosphatase in the obstructed kidney. In rats with unilateral ureteral obstruction release followed for 4 days with experimental acidosis induced by NH(4)Cl oral administration plasma pH and HCO(3)(-) were dramatically decreased in response to NH(4)Cl for 2 days compared with those in sham operated rats with acid loading, indicating a defect in H(+) excretion and HCO(3)(-) reabsorption after obstruction release. Expression of these transporters did not change in the contralateral nonobstructed kidney of rats with unilateral ureteral obstruction and unilateral ureteral obstruction release followed for 4 days. CONCLUSIONS: The expression of renal acid-base transporters is markedly decreased in the obstructed kidney, which may be responsible for the contribution of impaired renal H(+) excretion and HCO(3)(-) reabsorption to the urinary acidification defect in response to unilateral ureteral obstruction.",
author = "Guixian Wang and Troels Ring and Chunling Li and Kim, {Soo Wan} and Jianguo Wen and Djurhuus, {Jens Christian} and S{\o}ren Nielsen and J{\o}rgen Fr{\o}ki{\ae}r",
year = "2009",
doi = "10.1016/j.juro.2009.08.013",
language = "English",
volume = "182",
pages = "2964--73",
journal = "Journal of Urology",
issn = "0022-5347",
publisher = "Elsevier Inc.",
number = "6",

}

RIS

TY - JOUR

T1 - Unilateral Ureteral Obstruction Alters Expression of Acid-Base Transporters in Rat Kidney

AU - Wang, Guixian

AU - Ring, Troels

AU - Li, Chunling

AU - Kim, Soo Wan

AU - Wen, Jianguo

AU - Djurhuus, Jens Christian

AU - Nielsen, Søren

AU - Frøkiær, Jørgen

PY - 2009

Y1 - 2009

N2 - PURPOSE: Unilateral ureteral obstruction is a common clinical problem that is often associated with a urinary acidification defect caused by decreased net H(+) secretion and/or HCO(3)(-) reabsorption. To clarify the molecular mechanisms of these defects we examined expression levels of key acid-base transporters along the renal nephron segments and collecting duct. MATERIALS AND METHODS: Wistar rats (Møllegard Breeding Centre, Eiby, Denmark) underwent 24-hour unilateral ureteral obstruction, unilateral ureteral obstruction release followed for 4 days or unilateral ureteral obstruction release followed for 4 days plus experimental acidosis induced by NH(4)Cl oral administration. After sacrifice kidneys were processed for immunoblotting and immunohistochemistry. RESULTS: Semiquantitative immunoblotting revealed that unilateral ureteral obstruction caused significant mean +/- SE down-regulation of type 3 Na(+)/H(+) exchanger to 53% +/- 9%, electrogenic Na(+)/HCO(3)(-) cotransporter to 60% +/- 9%, type 1 bumetanide sensitive Na(+)-K(+)(NH(4)(+)) -2Cl(-) cotransporter to 64% +/- 7%, electroneutral Na(+)/HCO(3)(-) cotransporter to 43% +/- 4% and anion exchanger (pendrin) to 53% +/- 10% in the obstructed kidney, which was confirmed by immunohistochemistry. After release of unilateral ureteral obstruction down-regulation of these transporters persisted together with marked down-regulation of H(+)-adenosine triphosphatase in the obstructed kidney. In rats with unilateral ureteral obstruction release followed for 4 days with experimental acidosis induced by NH(4)Cl oral administration plasma pH and HCO(3)(-) were dramatically decreased in response to NH(4)Cl for 2 days compared with those in sham operated rats with acid loading, indicating a defect in H(+) excretion and HCO(3)(-) reabsorption after obstruction release. Expression of these transporters did not change in the contralateral nonobstructed kidney of rats with unilateral ureteral obstruction and unilateral ureteral obstruction release followed for 4 days. CONCLUSIONS: The expression of renal acid-base transporters is markedly decreased in the obstructed kidney, which may be responsible for the contribution of impaired renal H(+) excretion and HCO(3)(-) reabsorption to the urinary acidification defect in response to unilateral ureteral obstruction.

AB - PURPOSE: Unilateral ureteral obstruction is a common clinical problem that is often associated with a urinary acidification defect caused by decreased net H(+) secretion and/or HCO(3)(-) reabsorption. To clarify the molecular mechanisms of these defects we examined expression levels of key acid-base transporters along the renal nephron segments and collecting duct. MATERIALS AND METHODS: Wistar rats (Møllegard Breeding Centre, Eiby, Denmark) underwent 24-hour unilateral ureteral obstruction, unilateral ureteral obstruction release followed for 4 days or unilateral ureteral obstruction release followed for 4 days plus experimental acidosis induced by NH(4)Cl oral administration. After sacrifice kidneys were processed for immunoblotting and immunohistochemistry. RESULTS: Semiquantitative immunoblotting revealed that unilateral ureteral obstruction caused significant mean +/- SE down-regulation of type 3 Na(+)/H(+) exchanger to 53% +/- 9%, electrogenic Na(+)/HCO(3)(-) cotransporter to 60% +/- 9%, type 1 bumetanide sensitive Na(+)-K(+)(NH(4)(+)) -2Cl(-) cotransporter to 64% +/- 7%, electroneutral Na(+)/HCO(3)(-) cotransporter to 43% +/- 4% and anion exchanger (pendrin) to 53% +/- 10% in the obstructed kidney, which was confirmed by immunohistochemistry. After release of unilateral ureteral obstruction down-regulation of these transporters persisted together with marked down-regulation of H(+)-adenosine triphosphatase in the obstructed kidney. In rats with unilateral ureteral obstruction release followed for 4 days with experimental acidosis induced by NH(4)Cl oral administration plasma pH and HCO(3)(-) were dramatically decreased in response to NH(4)Cl for 2 days compared with those in sham operated rats with acid loading, indicating a defect in H(+) excretion and HCO(3)(-) reabsorption after obstruction release. Expression of these transporters did not change in the contralateral nonobstructed kidney of rats with unilateral ureteral obstruction and unilateral ureteral obstruction release followed for 4 days. CONCLUSIONS: The expression of renal acid-base transporters is markedly decreased in the obstructed kidney, which may be responsible for the contribution of impaired renal H(+) excretion and HCO(3)(-) reabsorption to the urinary acidification defect in response to unilateral ureteral obstruction.

U2 - 10.1016/j.juro.2009.08.013

DO - 10.1016/j.juro.2009.08.013

M3 - Journal article

C2 - 19846141

VL - 182

SP - 2964

EP - 2973

JO - Journal of Urology

JF - Journal of Urology

SN - 0022-5347

IS - 6

ER -