Recovery of Distal Nephron Enzyme Activity After Release of Unilateral Ureteral Obstruction

Vallés, Patricia G.; Merlo, V.; Berón, Walter; Manucha, Walter

doi:10.1016/s0022-5347(01)61987-6

Cited by 13 publications

(7 citation statements)

References 27 publications

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“…Together, this indicates a urinary acidification defect in BUO rats after release of the obstruction, consistent with the results of previous studies (2,37,38). BUO and release of BUO were associated with downregulation of several acid-base transporters in the proximal tubule and TAL.…”

Section: Discussionsupporting

confidence: 92%

“…This finding indicates development of a urinary acidification defect after release of the obstruction, as demonstrated previ- ously (2,3,15,37,38,41). Although measurements of urinary excretion of HCO 3 Ϫ and titratable acid would provide a more complete result, the present finding is consistent with previous studies demonstrating impaired urinary acidification in the kidney after obstruction (2,3,15,37,38,41).…”

Section: Metabolic Acidosis In Buo and Urinary Acidification Defect Asupporting

confidence: 91%

“…The urinary acidification defect associated with ureteral obstruction may gradually recover after release of the obstruction. Consistent with this, Valles and colleagues (38) showed recovery of both the ability to acidify urine and enzyme activity of H ϩ -ATPase in the distal nephron 30 days after release of 24-h unilateral ureteral obstruction. However, the pathophysiology of the urinary acidification defect after obstruction is complex, and the molecular mechanisms involved are still incompletely understood.…”

mentioning

confidence: 57%

“…The postobstructive acidification defects may be caused by both decreased protein abundance and enzyme activity. Consistent with this, Valles et al (38) demonstrated that the activity of H ϩ -ATPase was reduced in the medullary CD, causing a defect in urinary H ϩ excretion in rats with unilateral ureter obstruction, and Purcell et al (31) showed that changes in the cellular distribution of H ϩ -ATPase occur in intercalated cells throughout the CD after obstruction.…”

Section: Altered Expression Of H ϩ -Atpase In CD Of Rats With Buo Andmentioning

confidence: 80%

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Ureter obstruction alters expression of renal acid-base transport proteins in rat kidney

Wang¹,

Li²,

Kim³

et al. 2008

American Journal of Physiology-Renal Physiology

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Urinary tract obstruction impairs renal function and is often associated with a urinary acidification defect caused by diminished net H+ secretion and/or HCO3− 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+/HCO3− cotransporter (NBC1; 71 ± 5%), type 1 bumetanide-sensitive Na+-K+-2Cl− cotransporter (NKCC2; 3 ± 1%), electroneutral Na+/HCO3− 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 NH4Cl loading reduced plasma pH and HCO3− 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.

show abstract

Section: Discussionsupporting

confidence: 92%

Section: Metabolic Acidosis In Buo and Urinary Acidification Defect Asupporting

confidence: 91%

mentioning

confidence: 57%

Section: Altered Expression Of H ϩ -Atpase In CD Of Rats With Buo Andmentioning

confidence: 80%

See 2 more Smart Citations

Ureter obstruction alters expression of renal acid-base transport proteins in rat kidney

Wang¹,

Li²,

Kim³

et al. 2008

American Journal of Physiology-Renal Physiology

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show abstract

“…When the distal H + pumps are intact and animals excrete highly alkaline urine, urinary pCO 2 is increased by 2-to 4-fold from arterial pCO 2 (Dubose 1982;Gonzales et al 2004;Kim et al 2004). Several earlier studies of humans and experimental animals with acute ureteral obstruction demonstrated that the difference between urine and blood pCO 2 (U-B pCO 2 ) after bicarbonate loading was much lower in the obstructed kidney than the control kidney (Walls et al 1975;Ueda 1981;Dubose and Caflisch 1985;Valles et al 1999). Therefore, it was concluded that ureteral obstruction did suppress the capacity of the CD to secrete H + and reabsorb HCO 3 -, which led to development of distal renal tubular acidosis.…”

Section: Introductionmentioning

confidence: 99%

Pre- or post-treatment with aminoguanidine attenuates a renal distal acidification defect induced by acute ureteral obstruction in rats

Moosavi

Bagheri

Gheitasi

et al. 2013

Can. J. Physiol. Pharmacol.

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Acute unilateral ureteral obstruction (UUO) impairs distal nephron acid secretion and stimulates expression of inducible nitric oxide synthase (iNOS) in post-obstructed kidney (POK). This study investigated the influence of pre- or post-treatment with aminoguanidine as a selective iNOS inhibitor on UUO-induced renal functional disturbances. To induce acute UUO, the left ureter in rats was ligated and released after 24 h. Then, a 3 h clearance period followed by bicarbonate loading and thereafter a 30 min clearance period were allocated. Aminoguanidine was administered either prior to the UUO induction or after release of the obstruction in the different rat groups, while untreated and sham groups received normal saline. During the first clearance period, fractional bicarbonate excretion and urinary pH increased markedly in the POK of the untreated group compared with the left kidney of sham group, and a large drop in the difference between urine and blood pCO2 (U-B pCO2) was observed after bicarbonate loading; all of these parameters were ameliorated in the pre-treated and post-treated groups. However, the UUO-induced decreases in creatinine clearance, sodium reabsorption, urine osmolality, and free-water reabsorption in the POK were attenuated only in the post-treated group. Therefore, the in vivo application of a selective iNOS inhibitor partially improved the acute UUO-induced distal nephron acidification defect, while post-treatment but not pre-treatment with aminoguanidine ameliorated decrements of glomerular filtration, sodium reabsorption, and urine-concentrating ability.

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Hydronephrosis

Darrad¹,

Gupta²,

Rukin³

2019

Blandy's Urology

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Recovery of Distal Nephron Enzyme Activity After Release of Unilateral Ureteral Obstruction

Abstract: A correlation between the functional impairment of distal H+ secretion and decreased distal nephron enzyme activity has been shown. Recovery of both the functional and the enzyme activity at the distal nephron was demonstrated thirty days after obstruction release.

Cited by 13 publications

References 27 publications

Ureter obstruction alters expression of renal acid-base transport proteins in rat kidney

Ureter obstruction alters expression of renal acid-base transport proteins in rat kidney

Pre- or post-treatment with aminoguanidine attenuates a renal distal acidification defect induced by acute ureteral obstruction in rats

Hydronephrosis

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