Regulation by adrenal corticosteroids of sodium and potassium transport in loop of Henle and distal tubule of rat kidney.

Stanton, B A

doi:10.1172/jci112754

Cited by 76 publications

(30 citation statements)

References 38 publications

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“…[32][33][34][35][36] Because the pre-and postlosartan aldosterone levels were unchanged, we would not have expected a change in DTRNa. The observed increase in DTRNa, especially in the erect posture may be explained by an increased sensitivity to aldosterone (leading to loss of glomerulotubular balance).…”

Section: Discussionmentioning

confidence: 99%

The effect of single oral low-dose losartan on posture-related sodium handling in post-TIPS ascites-free cirrhosis

et al. 2006

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Post-TIPS ascites-free patients with cirrhosis and previous refractory ascites demonstrate subtle sodium retention when challenged with a high sodium load. This is also observed in pre-ascitic patients with cirrhosis. This phenomenon is dependent on an intrarenal angiotensin II (ANG II) mechanism related to the assumption of erect posture. We investigated whether similar mechanisms were involved in post-TIPS ascites-free patients, by studying 10 patients with functioning TIPS and no ascites. We measured the effect of changing from supine to erect posture on sodium excretion at baseline and after single oral low dose losartan (7.5 mg) which has been shown to blunt proximal and distal tubular sodium reabsorption in pre-ascites. At baseline, the assumption of erect posture produced a reduction in sodium excretion (from 0.30 ؎ 0.06 to 0.13 ؎ 0.02 mmol/min, P ‫؍‬ .05), which was mainly due to an increase in proximal tubular reabsorption of sodium (PTRNa) (69.7 ؎ 3.1% to 81.1 ؎ 1.8%, P ‫؍‬ .003). The administration of losartan resulted in a blunting of PTRNa (supine 69.7 ؎ 3.1% to 63.9 ؎ 3.9%, P ‫؍‬ .01 and erect 81.1 ؎ 1.8% to 73.8 ؎ 2.4%, P ‫؍‬ .01), accompanied by an increased distal tubular reabsorption of sodium in both postures, with no overall improvement in sodium excretion on standing. In conclusion, post-TIPS ascitesfree patients with cirrhosis exhibit erect posture-induced sodium retention. We speculate that (1) this effect is partly mediated by the effect of ANG II on PTRNa and (2) that the inability of low dose losartan to block the erect posture-induced sodium retention may be related to the erect posture-induced rise in aldosterone which is unmodified by losartan. (HEPATOLOGY 2006;44:640-649.)

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Section: Discussionmentioning

confidence: 99%

The effect of single oral low-dose losartan on posture-related sodium handling in post-TIPS ascites-free cirrhosis

et al. 2006

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“…The distal tubules possess regulated ion channels, which are involved in the reabsorption of sodium and bicarbonate ions from the urine in exchange for the excretion of potassium and hydrogen ions, thus rendering the urine acidic (33,34). This readsorption process is regulated by the hormone aldosterone, a ligand for the mineralocorticoid receptor involved in activation of genes involved in Na/H exchange (35,36).…”

Section: Discussionmentioning

confidence: 99%

The Winged Helix Transcriptional Activator HFH-3 Is Expressed in the Distal Tubules of Embryonic and Adult Mouse Kidney

Overdier¹,

Peterson

et al. 1997

Journal of Biological Chemistry

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The hepatocyte nuclear factor-3 (HNF-3)/fork head homolog (HFH) proteins are an extensive family of transcription factors, which share homology in the winged helix DNA binding domain. Members of the HFH/winged helix family have been implicated in cell fate determination during pattern formation, in organogenesis, and in cell-type-specific gene expression. In this study we isolated a full-length HFH-3 cDNA clone from a human kidney library which encoded a 351-amino acid protein containing a centrally located winged helix DNA binding domain. We demonstrate that HFH-3 is a potent transcriptional activator requiring 138 C-terminal residues for activity. We used in situ hybridization to demonstrate that HFH-3 expression is restricted to the epithelium of the renal distal convoluted tubules. We determined the HFH-3 DNA binding consensus sequence by in vitro DNA binding site selection using recombinant HFH-3 protein and used this consensus sequence to identify putative HFH-3 target genes expressed there. These putative HFH-3 target genes include the Na/KATPase, Na/H and anion exchangers, E-cadherin, and mineralocorticoid receptor genes as well as genes for the transcription factors HNF-1, vHNF-1, and HNF-4.Deciphering the mechanisms that lead to cell-specific gene transcription is critical for understanding cellular differentiation during mammalian embryogenesis. Differential expression of protein encoding genes occurs at the point of transcriptional initiation (1) and involves the assembly of several well characterized basal factors with TATA-binding protein, TATAbinding protein-associated factors, and RNA polymerase II at the initiation site of the promoter region (2). Promoter and enhancer regions are also composed of multiple DNA sites that interact with sequence-specific transcription factors, which are believed to enhance the recruitment of basal factors to the initiation complex. Cell-restricted gene expression thus relies upon the combinatorial recognition of multiple cis-acting DNA sequences bound by families of cell-specific nuclear factors, which potentiate or repress transcriptional initiation (3). Because transcription factors play a central role in regulating cellular differentiation, the analysis of their molecular structure and expression patterns has facilitated elucidation of regulatory pathways involved in establishing tissue-specific gene transcription. In combination with other cell-specific transcription factors, the hepatocyte nuclear factor-3␣ (HNF-3␣) 1 and -3␤ proteins regulate cell-specific transcription in hepatocytes (4) and in respiratory (5-8) and intestinal epithelium (9). The HNF-3/fork head homolog (HFH) proteins are an extensive family of transcription factors that share homology in the winged helix DNA binding domain (10

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“…This form of metabolic alkalosis is usually secondary to mineralocorticoid excess and requires K depletion to produce maximal alkalinization ofthe extracellular fluid (21)(22)(23). Chronic hyperaldosteronism or exogenous mineralocorticoid therapy results in a three-to fourfold increase in K secretion in the cortical CD and initial collecting tubule (24)(25)(26), although effects on urinary K excretion are relatively minor (24). If net K secretion in the cortical CD and initial collecting tubule exceeds K intake, profound K depletion would ensue unless there were a compensatory increase in K-absorptive flux in more terminal nephron segments.…”

Section: Discussionmentioning

confidence: 99%

Active proton secretion and potassium absorption in the rabbit outer medullary collecting duct. Functional evidence for proton-potassium-activated adenosine triphosphatase.

Wingo¹

1989

J. Clin. Invest.

132

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Regulation by adrenal corticosteroids of sodium and potassium transport in loop of Henle and distal tubule of rat kidney.

Abstract: Studies were conducted to examine the effects of adrenalectomy (ADX)

Cited by 76 publications

References 38 publications

The effect of single oral low-dose losartan on posture-related sodium handling in post-TIPS ascites-free cirrhosis

The effect of single oral low-dose losartan on posture-related sodium handling in post-TIPS ascites-free cirrhosis

The Winged Helix Transcriptional Activator HFH-3 Is Expressed in the Distal Tubules of Embryonic and Adult Mouse Kidney

Active proton secretion and potassium absorption in the rabbit outer medullary collecting duct. Functional evidence for proton-potassium-activated adenosine triphosphatase.

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