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  • 1
    Online Resource
    Online Resource
    Ureter obstruction alters expression of renal acid-base transport proteins in rat kidney
    American Physiological Society ; 2008
    In:  American Journal of Physiology-Renal Physiology Vol. 295, No. 2 ( 2008-08), p. F497-F506
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 295, No. 2 ( 2008-08), p. F497-F506
    Abstract: Urinary tract obstruction impairs renal function and is often associated with a urinary acidification defect caused by diminished net H + secretion and/or HCO 3 − reabsorption. To identify the molecular mechanisms of these defects, protein expression of key acid-base transporters were examined along the renal nephron and collecting duct of kidneys from rats subjected to 24-h bilateral ureteral obstruction (BUO), 4 days after release of BUO (BUO-R), or BUO-R rats with experimentally induced metabolic acidosis (BUO-A). Semiquantitative immunoblotting revealed that BUO caused a significant reduction in the expression of the type 3 Na + /H + exchanger (NHE3) in the cortex (21 ± 4%), electrogenic Na + /HCO 3 − cotransporter (NBC1; 71 ± 5%), type 1 bumetanide-sensitive Na + -K + -2Cl − cotransporter (NKCC2; 3 ± 1%), electroneutral Na + /HCO 3 − cotransporter (NBCn1; 46 ± 7%), and anion exchanger (pendrin; 87 ± 2%). The expression of H + -ATPase increased in the inner medullary collecting duct (152 ± 13%). These changes were confirmed by immunocytochemistry. In BUO-R rats, there was a persistent downregulation of all the acid-base transporters including H + -ATPase. Two days of NH 4 Cl loading reduced plasma pH and HCO 3 − levels in BUO-A rats. The results demonstrate that the expression of multiple renal acid-base transporters are markedly altered in response to BUO, which may be responsible for development of metabolic acidosis and contribute to the urinary acidification defect after release of the obstruction.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.00425.2007
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2008
    detail.hit.zdb_id: 1477287-5
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  • 2
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    Cyclooxygenase 2 inhibition exacerbates AQP2 and pAQP2 downregulation independently of V2 receptor abundance in the postobstructed kidney
    American Physiological Society ; 2010
    In:  American Journal of Physiology-Renal Physiology Vol. 298, No. 4 ( 2010-04), p. F941-F950
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 298, No. 4 ( 2010-04), p. F941-F950
    Abstract: Previously we demonstrated that ANG II receptor (AT1R) blockade attenuates V2 receptor (V2R), AQP2, and pS256-AQP2 downregulation in the postobstructed kidney and partially reverses obstruction-induced inhibition of cAMP generation and cyclooxygenase 2 (COX-2) induction. Therefore, we speculated whether the effects of AT1R blockade on V2R and the vasopressin-regulated pathway are attributable to attenuated COX-2 induction. To examine this, rats were subjected to 24-h bilateral ureteral obstruction (BUO) followed by 48-h release and treated with the COX-2 inhibitor parecoxib or saline. Control rats were sham-operated. Parecoxib treatment significantly reduced urine output 24 h after release of BUO whereas urine osmolality and solute-free water reabsorption was comparable between saline- and parecoxib-treated BUO rats. Immunoblotting revealed a significant decrease in AQP2 and pS256-AQP2 abundance to 20 and 23% of sham levels in parecoxib-treated BUO rats compared with 40 and 55% of sham levels in saline-treated BUO rats. Immunohistochemistry confirmed the exacerbated AQP2 and pS256-AQP2 downregulation in parecoxib-treated BUO rats. Finally, parecoxib treatment had no effect on V2R downregulation and the inhibited, vasopressin-stimulated cAMP generation in inner medullary membrane fractions from the postobstructed kidney. In conclusion, COX-2 inhibition exacerbates AQP2 and pS256-AQP2 downregulation 48 h after release of 24-h BUO independently of V2R abundance and vasopressin-stimulated cAMP generation. The results indicate that COX-2 inhibition does not mimic AT1R blockade-mediated effects and that AT1R-mediated AQP2 regulation in the postobstructed kidney collecting duct is independent of COX-2 induction.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.00605.2009
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2010
    detail.hit.zdb_id: 1477287-5
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  • 3
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    Online Resource
    Urinary tract obstruction induces transient accumulation of COX-2-derived prostanoids in kidney tissue
    American Physiological Society ; 2010
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 298, No. 4 ( 2010-04), p. R1017-R1025
    Details
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 298, No. 4 ( 2010-04), p. R1017-R1025
    Abstract: Inhibitors of cyclooxygenase (COX)-2 prevent suppression of aquaporin-2 and reduce polyuria in the acute phase after release of bilateral ureteral obstruction (BUO). We hypothesized that BUO leads to COX-2-mediated local accumulation of prostanoids in inner medulla (IM) tissue. To test this, rats were subjected to BUO and treated with selective COX-1 or COX-2 inhibitors. Tissue was examined at 2, 6, 12, and 24 h after BUO. COX-2 protein abundance increased in IM 12 and 24 h after onset of BUO but did not change in cortex. COX-1 did not change at any time points in any region. A full profile of all five primary prostanoids was obtained by mass spectrometric determination of PGE 2 , PGF 2α , 6-keto-PGF 1α , PGD 2 , and thromboxane (Tx) B 2 concentrations in kidney cortex/outer medulla and IM fractions. IM concentration of PGE 2 , 6-keto-PGF 1α , and PGF 2α was increased at 6 h BUO, and PGE 2 and PGF 2α increased further at 12 h BUO. TxB 2 increased after 12 h BUO. 6-keto-PGF 1α remained significantly increased after 24 h BUO. The COX-2 inhibitor parecoxib lowered IM PGE 2, TxB 2 , 6-keto-PGF 1α , and PGF 2α below vehicle-treated BUO and sham rats at 6, 12 and, 24 h BUO. The COX-1 inhibitor SC-560 lowered PGE 2 , PGF 2α , and PGD 2 in IM compared with untreated 12 h BUO, but levels remained significantly above sham. In cortex tissue, PGE 2 and 6-keto-PGF 1α concentrations were elevated at 6 h only. In conclusion, COX-2 activity contributes to the transient increase in prostacyclin metabolite 6-keto-PGF 1α and TxB 2 concentration in the kidney IM, and COX-2 is the predominant isoform that is responsible for accumulation of PGE 2 and PGF 2α with minor, but significant, contributions from COX-1. PGD 2 synthesis is mediated exclusively by COX-1. In BUO, therapeutic interventions aimed at the COX-prostanoid pathway should target primarily COX-2.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    URL: Article
    DOI: 10.1152/ajpregu.00336.2009
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2010
    detail.hit.zdb_id: 1477297-8
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  • 4
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    Online Resource
    Candesartan prevents long-term impairment of renal function in response to neonatal partial unilateral ureteral obstruction
    American Physiological Society ; 2007
    In:  American Journal of Physiology-Renal Physiology Vol. 292, No. 2 ( 2007-02), p. F736-F748
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 292, No. 2 ( 2007-02), p. F736-F748
    Abstract: Angiotensin II (ANG II) plays an important role in the development of obstructive nephropathy. Here, we examined the effects of the ANG II receptor type 1 (AT1R) blockade using candesartan on long-term renal molecular and functional changes in response to partial unilateral ureteral obstruction (PUUO). Newborn rats were subjected to severe PUUO or sham operation (Sham) within the first 48 h of life. Candesartan was provided in the drinking water (10 mg·kg −1 ·day −1 ) from day 21 of life until 10 wk of age. Renal blood flow (RBF) was evaluated by MRI, glomerular filtration rate (GFR) was measured using the renal clearance of 51 Cr-EDTA, and the renal expression of Na-K-ATPase and the collecting duct water channel aquaporin-2 (AQP2) was examined by immunoblotting and immunocytochemistry. At 10 wk of age, PUUO significantly reduced RBF (0.8 ± 0.1 vs. 1.6 ± 0.1 ml·min −1 ·100 g body wt −1 ; P 〈 0.05) and GFR (37 ± 16 vs. 448 ± 111 μl·min −1 ·100 g body wt −1 ; P 〈 0.05) compared with Sham. Candesartan prevented the RBF reduction (PUUO+CAN: 1.6 ± 0.2 vs. PUUO: 0.8 ± 0.1 ml·min −1 ·100 g body wt −1 ; P 〈 0.05) and attenuated the GFR reduction (PUUO+CAN: 265 ± 68 vs. PUUO: 37 ± 16 μl·min −1 ·100 g body wt −1 ; P 〈 0.05). PUUO was also associated with a significant downregulation in the expression of Na-K-ATPase (75 ± 12 vs. 100 ± 5%, P 〈 0.05) and AQP2 (52 ± 15 vs. 100 ± 4%, P 〈 0.05), which were also prevented by candesartan (Na-K-ATPase: 103 ± 8 vs. 100 ± 5% and AQP2: 74 ± 13 vs. 100 ± 4%). These findings were confirmed by immunocytochemistry. Consistent with this, candesartan treatment partly prevented the reduction in solute free water reabsorption and attenuated fractional sodium excretion in rats with PUUO. In conclusion, candesartan prevents or attenuates the reduction in RBF, GFR and dysregulation of AQP2 and Na-K-ATPase in response to congenital PUUO in rats, suggesting that AT1R blockade may protect the neonatally obstructed kidney against development of obstructive nephropathy.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.00241.2006
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2007
    detail.hit.zdb_id: 1477287-5
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  • 5
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    Bilateral ureteral obstruction induces early downregulation and redistribution of AQP2 and phosphorylated AQP2
    American Physiological Society ; 2011
    In:  American Journal of Physiology-Renal Physiology Vol. 301, No. 1 ( 2011-07), p. F226-F235
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 301, No. 1 ( 2011-07), p. F226-F235
    Abstract: Bilateral ureteral obstruction (BUO) is characterized by impairment of urine flow from the kidneys and altered expression of specific membrane proteins in the kidney involved in regulation of renal water and salt transport. Importantly, 24-h BUO reduces the abundance of the collecting duct water channel aquaporin-2 (AQP2) and AQP2 phosphorylated at serine 256 (AQP2pS256). To investigate the mechanism behind downregulation of AQP2 in BUO, rats were subjected to BUO and examined after 2, 6, 12, and 24 h. Q-PCR and immunoblotting showed significantly decreased AQP2 mRNA expression after 2-h BUO and decreased abundance of total AQP2 after 12 and 24 h. In parallel, immunohistochemistry showed weaker labeling of AQP2 at the apical surface of inner medullary collecting ducts (IMCD) compared with controls. The abundance of AQP2pS256 was significantly reduced from 6-h BUO and was confirmed by immunohistochemistry. Importantly, immunoblotting showed reduced abundance of AQP2pS261 after 12- and 24-h BUO mimicking total AQP2. Immunohistochemistry demonstrated early changed intracellular localization of AQP2pS261 in BUO, and colocalization studies showed redistribution from the apical membrane to early endosomes and lysosomes. In conclusion, BUO induces a very early regulation of AQP2 both at the level of abundance and on cellular localization. AQP2 and AQP2 phosphorylated at ser261 redistribute to more intracellular localizations and colocalize with the early endosomal marker EEA1 and the lysosomal marker cathepsin D, suggesting that early downregulation of AQP2 could in part be caused by degradation of AQP2 through a lysosomal degradation pathway.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.00664.2010
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2011
    detail.hit.zdb_id: 1477287-5
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