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Rapid stimulation of human renal ENaC by cAMP in Xenopus laevis oocytes.
Robins GG
,
MacLennan KA
,
Boot-Handford RP
,
Sandle GI
.
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Among the compensatory mechanisms restoring circulating blood volume after severe haemorrhage, increased vasopressin secretion enhances water permeability of distalnephron segments and stimulates Na(+) reabsorption in cortical collecting tubules via epithelial sodium channels (ENaC). The ability of vasopressin to upregulate ENaC via a cAMP-dependent mechanism in the medium to long term is well established. This study addressed the acute regulatory effect of cAMP on human ENaC (hENaC) and thus the potential role of vasopressin in the initial compensatory responses to haemorrhagic shock. The effects of raising intracellular cAMP (using 5 mmol/L isobutylmethylxanthine (IBMX) and 50 μmol/L forskolin) on wild-type and Liddle-mutated hENaC activity expressed in Xenopus oocytes and hENaC localisation in oocyte membranes were evaluated by dual-electrode voltage clamping and immunohistochemistry, respectively. After 30 min, IBMX + forskolin had stimulated amiloride-sensitive Na(+) current by 52% and increased the membrane density of Na(+) channels in oocytes expressing wild-type hENaC. These responses were prevented by 5 μmol/L brefeldin A, which blocks antegrade vesicular transport. By contrast, IBMX + forskolin had no effects in oocytes expressing Liddle-mutated hENaC. cAMP stimulated rapid, exocytotic recruitment of wild-type hENaC into Xenopus oocyte membranes, but had no effect on constitutively over-expressed Liddle-mutated hENaC. Extrapolating these findings to the early cAMP-mediated effect of vasopressin on cortical collecting tubule cells, they suggest that vasopressin rapidly mobilises ENaC to the apical membrane of cortical collecting tubule cells, but does not enhance ENaC activity once inserted into the membrane. We speculate that this stimulatory effect on Na(+) reabsorption (and hence water absorption) may contribute to the early restoration of extracellular fluid volume following severe haemorrhage.
Abriel,
Feedback inhibition of rat amiloride-sensitive epithelial sodium channels expressed in Xenopus laevis oocytes.
1999, Pubmed,
Xenbase
Abriel,
Feedback inhibition of rat amiloride-sensitive epithelial sodium channels expressed in Xenopus laevis oocytes.
1999,
Pubmed
,
Xenbase
Alfaidy,
Vasopressin potentiates mineralocorticoid selectivity by stimulating 11 beta hydroxysteroid deshydrogenase in rat collecting duct.
1997,
Pubmed
Auberson,
Epithelial Na+ channel mutants causing Liddle's syndrome retain ability to respond to aldosterone and vasopressin.
2003,
Pubmed
Awayda,
Regulation of the epithelial Na(+) channel by intracellular Na(+).
1999,
Pubmed
,
Xenbase
Awayda,
Protein kinase regulation of a cloned epithelial Na+ channel.
1996,
Pubmed
,
Xenbase
Benos,
Structure and function of amiloride-sensitive Na+ channels.
1995,
Pubmed
Bubien,
Liddle's disease: abnormal regulation of amiloride-sensitive Na+ channels by beta-subunit mutation.
1996,
Pubmed
Butterworth,
Acute ENaC stimulation by cAMP in a kidney cell line is mediated by exocytic insertion from a recycling channel pool.
2005,
Pubmed
Canessa,
Amiloride-sensitive epithelial Na+ channel is made of three homologous subunits.
1994,
Pubmed
,
Xenbase
Canessa,
Epithelial sodium channel related to proteins involved in neurodegeneration.
1993,
Pubmed
,
Xenbase
Chraïbi,
Dual effect of temperature on the human epithelial Na+ channel.
2003,
Pubmed
,
Xenbase
Collier,
Identification of epithelial Na+ channel (ENaC) intersubunit Cl- inhibitory residues suggests a trimeric alpha gamma beta channel architecture.
2011,
Pubmed
,
Xenbase
Dijkink,
The epithelial sodium channel (ENaC) is intracellularly located as a tetramer.
2002,
Pubmed
,
Xenbase
Ecelbarger,
Vasopressin-mediated regulation of epithelial sodium channel abundance in rat kidney.
2000,
Pubmed
Firsov,
The heterotetrameric architecture of the epithelial sodium channel (ENaC).
1998,
Pubmed
,
Xenbase
Fushimi,
Phosphorylation of serine 256 is required for cAMP-dependent regulatory exocytosis of the aquaporin-2 water channel.
1997,
Pubmed
Hansson,
Hypertension caused by a truncated epithelial sodium channel gamma subunit: genetic heterogeneity of Liddle syndrome.
1995,
Pubmed
,
Xenbase
Kellenberger,
Mutations causing Liddle syndrome reduce sodium-dependent downregulation of the epithelial sodium channel in the Xenopus oocyte expression system.
1998,
Pubmed
,
Xenbase
Kosari,
Subunit stoichiometry of the epithelial sodium channel.
1998,
Pubmed
,
Xenbase
Marunaka,
Effects of vasopressin and cAMP on single amiloride-blockable Na channels.
1991,
Pubmed
Nicco,
Chronic exposure to vasopressin upregulates ENaC and sodium transport in the rat renal collecting duct and lung.
2001,
Pubmed
Niisato,
cAMP stimulates Na(+) transport in rat fetal pneumocyte: involvement of a PTK- but not a PKA-dependent pathway.
1999,
Pubmed
Reif,
Sodium transport by rat cortical collecting tubule. Effects of vasopressin and desoxycorticosterone.
1986,
Pubmed
Schafer,
cAMP mediates the increase in apical membrane Na+ conductance produced in rat CCD by vasopressin.
1990,
Pubmed
Schild,
A mutation in the epithelial sodium channel causing Liddle disease increases channel activity in the Xenopus laevis oocyte expression system.
1995,
Pubmed
,
Xenbase
Shimkets,
Liddle's syndrome: heritable human hypertension caused by mutations in the beta subunit of the epithelial sodium channel.
1994,
Pubmed
Shimkets,
In vivo phosphorylation of the epithelial sodium channel.
1998,
Pubmed
Shimkets,
The activity of the epithelial sodium channel is regulated by clathrin-mediated endocytosis.
1997,
Pubmed
,
Xenbase
Snyder,
cAMP and serum and glucocorticoid-inducible kinase (SGK) regulate the epithelial Na(+) channel through convergent phosphorylation of Nedd4-2.
2004,
Pubmed
Snyder,
Liddle's syndrome mutations disrupt cAMP-mediated translocation of the epithelial Na(+) channel to the cell surface.
2000,
Pubmed
Snyder,
Mechanism by which Liddle's syndrome mutations increase activity of a human epithelial Na+ channel.
1995,
Pubmed
,
Xenbase
Stewart,
Atomic force microscopy reveals the architecture of the epithelial sodium channel (ENaC).
2011,
Pubmed
,
Xenbase
Stockand,
Insight toward epithelial Na+ channel mechanism revealed by the acid-sensing ion channel 1 structure.
2008,
Pubmed
