Renal Acidification: Cellular Mechanisms of Tubular Transport and Regulation

Alpern, Robert J.; Rector, Floyd C.

doi:10.1002/cphy.cp080118

Cited by 4 publications

(5 citation statements)

References 199 publications

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“…NaCl absorption in this segment is mediated by an Na/H antiporter functioning in parallel with a Cl/base exchanger (1,2). A number of physiologic regulators of NaCl absorption, such as angiotensin II, endothelin, dopamine, and adrenergic catecholamines have been demonstrated to regulate NaCl absorption through regulation of the apical membrane Na/H antiporter (3). While five mammalian Na/H antiporter gene isoforms have been cloned (4)(5)(6)(7)(8)(9), present evidence suggests that a major fraction of apical membrane Na/H exchange mediating transepithelial transport is encoded by Na/H exchanger 3 (NHE3) 1 (10,11).…”

Section: Introductionmentioning

confidence: 99%

Chronic hyperosmolality increases NHE3 activity in OKP cells.

Ambühl¹,

Amemiya²,

Preisig³

et al. 1998

J. Clin. Invest.

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This study investigated the effect of chronic hypertonicity on the OKP cell Na/H antiporter, encoded by Na/H exchanger 3 (NHE3). Chronic (48 h) increases in extracellular glucose, mannitol, or raffinose concentration caused a significant increase in Na/H antiporter activity, while increases in urea concentration were without effect. This effect was seen with changes in osmolality of only 20 mOsm/liter, a magnitude that is observed clinically in poorly controlled diabetes mellitus. Increases in mannitol concentration acutely inhibited and chronically stimulated Na/H antiporter activity. The increase in Na/H antiporter activity induced by hypertonic incubation was resistant to 10(-7) and 5 x 10(-6) M but inhibited by 10(-4) M ethylisopropyl amiloride, consistent with regulation of NHE3. In addition, hypertonicity increased total cellular and plasma membrane NHE3 protein abundance twofold, with only a small increase in NHE3 mRNA abundance. We conclude that chronic pathophysiologically relevant increases in tonicity lead to increases in NHE3 protein abundance and activity. This may be responsible for increased proximal tubule apical membrane Na/H antiporter activity in poorly controlled diabetes mellitus, which could then contribute to hypertension, glomerular hyperfiltration and diabetic nephropathy.

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Section: Introductionmentioning

confidence: 99%

Chronic hyperosmolality increases NHE3 activity in OKP cells.

Ambühl¹,

Amemiya²,

Preisig³

et al. 1998

J. Clin. Invest.

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“…Acidic environment which is typical of tubular urine promotes free radical production [ 163 ] while high pH of normal extracellular fluid inhibits it [ 164 , 165 ]. Since CM administration increases the oxidative stress and increases generation of free radicals and reactive oxygen species (ROS), alkalinizing renal tubular fluid with bicarbonate seems a logical strategy to reduce renal injury [ 166 ].…”

Section: Prevention Of Ci-akimentioning

confidence: 99%

Radiographic Contrast-Media-Induced Acute Kidney Injury: Pathophysiology and Prophylactic Strategies

Sadat

2013

ISRN Radiology

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Contrast-induced acute kidney injury (CI-AKI) is one of the most widely discussed and debated topics in cardiovascular medicine. With increasing number of contrast-media- (CM-) enhanced imaging studies being performed and growing octogenarian population with significant comorbidities, incidence of CI-AKI remains high. In this review, pathophysiology of CI-AKI, its relationship with different types of CM, role of serum and urinary biomarkers for diagnosing CI-AKI, and various prophylactic strategies used for nephroprotection against CI-AKI are discussed in detail.

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“…These ectodomains are expressed by exons [17][18][19]. Within this region, a mutation on exon 17 (16073CrT) and one on intron 18 (18053CrT) were found with allele frequencies of 5.4% and 1.9%, respectively.…”

Section: Resequencingmentioning

confidence: 99%

“…The kidney isoform is transcribed from an alternate promoter located within intron 3 of the AE1 gene (SLC4A1, EPB3) and lacks the N-terminal amino acid residues of the erythroid AE1 protein [16]. Truncated AE1 is involved in renal-acid secretion through its transporting bicarbonate ions into the blood by exchange with chloride ions, and an H + /K + ATPase secretes hydrogen ions into the urine [17].…”

mentioning

confidence: 99%

Promoter Polymorphism of the Anion‐Exchange Protein 1 Associated with Severe Malarial Anemia and Fatality

et al. 2006

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The anion-exchange protein 1 (AE1 or band 3) is involved in the erythrocyte invasion of the malaria parasite Plasmodium falciparum, the adhesion of infected erythrocytes to endothelial cells, and the regulation of acid-base homeostasis, which is a critical factor for human survival in severe malaria. A variant of the AE1 gene promoter 512 base pairs (bp) distant from the transcription start site and 5699 bp from the translation start codon (AE1(-5699T-->C)) has been shown to be highly frequent in a population from the Ashanti region, Ghana. In a matched-pair case-control study (736 pairs), children heterozygous for the mutation (AE1(-5699CT)) had an increased risk of severe malarial anemia (odds ratio [OR], 1.45 [95% confidence interval {CI}, 1.05-2.01]; P<.03). In children who developed this complication, carriers of the mutation AE1(-5699C) had a higher fatality rate than those with the genotype AE1(-5699TT) (relative risk, 7.1 [95% CI, 1.0-52.8]). Moreover, in children with cerebral malaria, AE1(-5699C) was positively associated with a distinctive metabolic acidosis (P<.002), and results of luciferase assays showed higher transcriptional activity of the AE1(-5699C) allele. These results demonstrate that the AE1 promoter allele might influence the infection phenotype and the risk of fatal outcome in children with severe malaria. In this regard, a crucial role of the AE1 protein in malaria is emphasized.

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Renal Acidification: Cellular Mechanisms of Tubular Transport and Regulation

Abstract: The sections in this article are: Newer Techniques Carbonic Anhydrase Mechanisms of Proximal Tubular Acidification Apical Membrane Basolateral Membrane Leak Pathways Carbonic Anhydrase Summary … Show more

Cited by 4 publications

References 199 publications

Chronic hyperosmolality increases NHE3 activity in OKP cells.

Chronic hyperosmolality increases NHE3 activity in OKP cells.

Radiographic Contrast-Media-Induced Acute Kidney Injury: Pathophysiology and Prophylactic Strategies

Promoter Polymorphism of the Anion‐Exchange Protein 1 Associated with Severe Malarial Anemia and Fatality

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