Chronic Exposure to Vasopressin Upregulates ENaC and Sodium Transport in the Rat Renal Collecting Duct and Lung

Nicco, Carole; Wittner, Monika; DiStefano, Antonio; Jounier, Sylvie; Bankir, Lise; Bouby, Nadine

doi:10.1161/hy1001.092641

Cited by 111 publications

(101 citation statements)

References 39 publications

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“…It has been shown recently that vasopressin not only has an acute impact on ENaC-dependent sodium transport (Tomita et al, 1985;Verrey, 1994;Blot-Chabaud et al, 1996;Djelidi et al, 1997) but also has a delayed effect on the expression of b and gENaC subunits, in the kidney, by activating the V2 receptors (Ecelbarger et al, 2000;Nicco et al, 2001) (Figure 3). This effect is accompanied by a significant increase in sodium and water transport (Nicco et al, 2001) (Figure 4), suggesting associated changes in functional ENaC membrane proteins. Interestingly, an increase in the mRNA expression of b and gENaC subunits has also been observed in the lung of rats with either chronic water restriction or chronic infusion of a vasopressin V2 receptor agonist.…”

Section: Renal Consequences Of a High Level Of Vasopressin In A Healtmentioning

confidence: 99%

“…Interestingly, an increase in the mRNA expression of b and gENaC subunits has also been observed in the lung of rats with either chronic water restriction or chronic infusion of a vasopressin V2 receptor agonist. The concomitant decrease in extrarenal water losses (water intake minus urine flow rate) suggests indirectly that mRNA upregulation is followed by an increase in functional channels and sodium transport and, consequently, in the reabsorption of water (Nicco et al, 2001).…”

Section: Renal Consequences Of a High Level Of Vasopressin In A Healtmentioning

confidence: 99%

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Mild dehydration, vasopressin and the kidney: animal and human studies

Bouby

Fernandes

2003

Eur J Clin Nutr

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Water balance depends essentially on fluid intake and urine excretion. Mild dehydration and the consequent hypertonicity of the extracellular fluid induce an increase in vasopressin secretion, thus stimulating urine concentrating processes and the feeling of thirst. The osmotic threshold for the release of vasopressin is lower than that for thirst and also shows appreciable individual variation. Sustained high levels of vasopressin and low hydration induce morphological and functional changes in the kidney. However, they could also be risk factors in several renal disorders, such as chronic renal failure, diabetic nephropathy and saltsensitive hypertension.

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Section: Renal Consequences Of a High Level Of Vasopressin In A Healtmentioning

confidence: 99%

Section: Renal Consequences Of a High Level Of Vasopressin In A Healtmentioning

confidence: 99%

Mild dehydration, vasopressin and the kidney: animal and human studies

Bouby

Fernandes

2003

Eur J Clin Nutr

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“…Yet, in a recent study (25), it was reported that chronic infusion of DDAVP in Brattleboro and in Sprague-Dawley rats led to increases in ENaC mRNA expression in the lung and in the renal cortex. Clearly, many other hormones and autacoids such as adrenaline and prostaglandins increase cAMP in airway and alveolar epithelia and directly or indirectly regulate Na ϩ transport (15,32).…”

Section: Discussionmentioning

confidence: 98%

“…DDAVP, a selective V2 receptor agonist, increases ␤-and ␥-ENaC expression in the renal cortex and in a collecting duct cell line, RCCD1 (9,10,25). In Brattleboro rats, a rodent model of central diabetes insipidus, DDAVP infusion increases ␤-ENaC and several other target genes in the renal inner medulla (5).…”

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confidence: 99%

AVP-induced VIT32 gene expression in collecting duct cells occurs via trans-activation of a CRE in the 5′-flanking region of the VIT32 gene

Thomas

Loftus

Liu

2004

American Journal of Physiology-Renal Physiology

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. AVP-induced VIT32 gene expression in collecting duct cells occurs via trans-activation of a CRE in the 5Ј-flanking region of the VIT32 gene. Am J Physiol Renal Physiol 287: F460 -F468, 2004. First published May 12, 2004 10.1152/ajprenal.00107.2004.-VIT32, a vasopressin-induced transcript, inhibits Na ϩ transport when coexpressed with the epithelial sodium channel in Xenopus laevis oocytes (EMBO J 21: 5109 -5117, 2002). To understand the mechanism of VIT32 gene regulation, we examined the effect of DDAVP and cAMP stimulation on VIT32 expression in M-1 mouse collecting duct cells and in H441 human airway epithelial cells. Elevation of cAMP with forskolin and IBMX increased VIT32 gene expression with a peak effect at 2 h. The increase in gene expression was abolished by H89 and by actinomycin D, suggesting that cAMP stimulates VIT32 mRNA expression by a PKA-mediated increase in gene transcription. An ϳ1.5-kb fragment of the 5Ј-flanking region of VIT32 was cloned and was able to confer cAMP-stimulated reporter gene activity when transfected into M-1 and H441 cells. By deletion analysis and sitedirected mutagenesis, a cAMP response element (CRE) was identified within the proximal promoter region that was sufficient to account for the increase in VIT32 gene expression seen with DDAVP and elevation of cAMP. Furthermore, DDAVP-stimulated VIT32 promoterreporter activity was inhibited by H89 and by a dominant negative CREB construct. Finally, we were able to identify CREB as a nuclear protein that bound to the VIT32 CRE in gel mobility shift assays. In summary, DDAVP stimulates transcription of VIT32 via a CRE within the proximal promoter region of the VIT32 gene.PP5395; epithelial sodium channel; sodium transport; airway epithelia; adenosine 3Ј,5Ј-cyclic monophosphate response element binding protein IN THE COLLECTING duct, AVP binds the V2 receptor and regulates water homeostasis by activation of the water channel, aquaporin-2 (34). AVP also regulates Na ϩ handling in the distal nephron by its effects on Na ϩ transporters (30). The principal effect is a stimulation of benzamil-sensitive Na ϩ transport, which has been noted in the toad bladder, in the isolated rat cortical collecting duct, in primary cultures of collecting duct cells, and in many distal nephron cell lines. The early effects of AVP may be mediated by cAMP and result in an increase in surface expression of the epithelial Na ϩ channel (ENaC) (24,31,35). Others have reported an increase in Na ϩ -K ϩ -ATPase activity in microdissected mouse and rat collecting ducts and in a mouse collecting duct cell line, mpkCCD14 (6,8,13). In A6 cells, an amphibian cell line used as a model of collecting duct epithelia, the early effects of AVP effect on Na ϩ transport appear to require phosphatidylinositol-3 kinase and be mediated by the regulatory kinase sgk1 (2,11,12).Although the earliest effects of AVP on Na ϩ transport are independent of transcription, chronic effects are likely to require the transcription of target genes (18). DDAVP, a selective V2 receptor agoni...

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“…Given these data and data from other studies (11), it has been postulated that a chronically low fluid intake leads to elevated vasopressin levels and increased GFR via tubuloglomerular feedback mechanisms and hyperfiltration. Decreased sodium excretion would theoretically also occur due to vasopressin upregulation of amiloride-sensitive epithelial sodium channels (12). Over a prolonged period of time, these combined factors could translate to heightened risk for GFR loss.…”

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confidence: 99%