scholarly journals Regulated sodium transport in the renal connecting tubule (CNT) via the epithelial sodium channel (ENaC)

2009 ◽  
Vol 458 (1) ◽  
pp. 111-135 ◽  
Author(s):  
Johannes Loffing ◽  
Christoph Korbmacher
Keyword(s):  
Sodium Channel ◽  
Sodium Transport ◽  
Epithelial Sodium Channel ◽  
Connecting Tubule ◽  
Epithelial Sodium Channel Enac

scholarly journals Prostaglandin E2 stimulates the epithelial sodium channel (ENaC) in cultured mouse cortical collecting duct cells in an autocrine manner

2020 ◽  
Vol 152 (8) ◽  
Author(s):  
Morag K. Mansley ◽  
Christian Niklas ◽  
Regina Nacken ◽  
Kathrin Mandery ◽  
Hartmut Glaeser ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Prostaglandin E2 ◽  
Sodium Channel ◽  
Sodium Transport ◽  
Collecting Duct ◽  
Epithelial Sodium Channel ◽  
Prostaglandin E ◽  
Cortical Collecting Duct ◽  
Transepithelial Sodium Transport ◽  
Epithelial Sodium Channel Enac

Prostaglandin E2 (PGE2) is the most abundant prostanoid in the kidney, affecting a wide range of renal functions. Conflicting data have been reported regarding the effects of PGE2 on tubular water and ion transport. The amiloride-sensitive epithelial sodium channel (ENaC) is rate limiting for transepithelial sodium transport in the aldosterone-sensitive distal nephron. The aim of the present study was to explore a potential role of PGE2 in regulating ENaC in cortical collecting duct (CCD) cells. Short-circuit current (ISC) measurements were performed using the murine mCCDcl1 cell line known to express characteristic properties of CCD principal cells and to be responsive to physiological concentrations of aldosterone and vasopressin. PGE2 stimulated amiloride-sensitive ISC via basolateral prostaglandin E receptors type 4 (EP4) with an EC50 of ∼7.1 nM. The rapid stimulatory effect of PGE2 on ISC resembled that of vasopressin. A maximum response was reached within minutes, coinciding with an increased abundance of β-ENaC at the apical plasma membrane and elevated cytosolic cAMP levels. The effects of PGE2 and vasopressin were nonadditive, indicating similar signaling cascades. Exposing mCCDcl1 cells to aldosterone caused a much slower (∼2 h) increase of the amiloride-sensitive ISC. Interestingly, the rapid effect of PGE2 was preserved even after aldosterone stimulation. Furthermore, application of arachidonic acid also increased the amiloride-sensitive ISC involving basolateral EP4 receptors. Exposure to arachidonic acid resulted in elevated PGE2 in the basolateral medium in a cyclooxygenase 1 (COX-1)–dependent manner. These data suggest that in the cortical collecting duct, locally produced and secreted PGE2 can stimulate ENaC-mediated transepithelial sodium transport.

scholarly journals Early effect of aldosterone on the rate of synthesis of the epithelial sodium channel alpha subunit in A6 renal cells.

1997 ◽  
Vol 8 (12) ◽  
pp. 1813-1822 ◽  
Author(s):  
A May ◽  
A Puoti ◽  
H P Gaeggeler ◽  
J D Horisberger ◽  
B C Rossier
Keyword(s):  
Sodium Channel ◽  
Sodium Transport ◽  
Epithelial Sodium Channel ◽  
Mrna Abundance ◽  
Alpha Subunit ◽  
Gamma Subunit ◽  
Early Effect ◽  
Alpha Beta ◽  
Epithelial Sodium Channel Enac ◽  
In Cells

Transepithelial Na+ reabsorption across tight epithelia is regulated by aldosterone. The amiloride-sensitive epithelial sodium channel (ENaC) is a major target for the natriferic action of aldosterone. In this study, the effect of aldosterone on ENaC mRNA abundance and the rate of protein synthesis for each of the three ENaC subunits (alpha, beta and gamma) in the A6 kidney cell line were examined. In cells grown on plastic, aldosterone induced a large and rapid increase in epithelial sodium channel (ENaC) beta and gamma subunit mRNA abundance, but this effect is not translated into the synthesis of the corresponding proteins. In cells grown on a porous substrate, amiloride-sensitive electrogenic sodium transport was expressed and was upregulated by aldosterone (300 nM) as early as 1 h after the addition of the hormone. The alpha, beta, and gamma mRNA abundance was not changed by aldosterone during the first 3 h of stimulation, whereas a fourfold increase over control was observed after 24 h. The rate of synthesis of alpha subunit was significantly increased above control already 60 min after aldosterone addition, whereas beta subunit synthesis increased only 6 h after hormone addition, with no significant change for the gamma subunit. The half-lives of each subunit as assessed by 35S methionine pulse-chase experiments were short (between 40 and 50 min) and were not modified by aldosterone. Taking into account the short half-life of ENaC protein and assuming that the synthesis of the alpha subunit is a limiting factor in the assembly and expression of new channels at the cell surface, it is proposed that the aldosterone regulation of sodium transport might be, in part, mediated by de novo synthesis of the channel protein.

scholarly journals Inactivation of the epithelial sodium channel (ENaC) in the aldosterone‐sensitive connecting tubule

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Søren Brandt Poulsen ◽  
Jeppe Praetorius ◽  
Lance Miller ◽  
Raoul Nelson ◽  
Bernard Rossier ◽  
...  
Keyword(s):  
Sodium Channel ◽  
Epithelial Sodium Channel ◽  
Connecting Tubule ◽  
Epithelial Sodium Channel Enac

scholarly journals Ankyrin G Expression Regulates Apical Delivery of the Epithelial Sodium Channel (ENaC)

2016 ◽  
Vol 292 (1) ◽  
pp. 375-385 ◽  
Author(s):  
Christine A. Klemens ◽  
Robert S. Edinger ◽  
Lindsay Kightlinger ◽  
Xiaoning Liu ◽  
Michael B. Butterworth
Keyword(s):  
Sodium Channel ◽  
Epithelial Sodium Channel ◽  
Ankyrin G ◽  
Epithelial Sodium Channel Enac

The epithelial sodium channel (ENaC) is intracellularly located as a tetramer

2002 ◽  
Vol 444 (4) ◽  
pp. 549-555 ◽  
Author(s):  
Lisette Dijkink ◽  
Anita Hartog ◽  
René Bindels ◽  
Carel van Os
Keyword(s):  
Sodium Channel ◽  
Epithelial Sodium Channel ◽  
Epithelial Sodium Channel Enac

Differential Regulation of the Epithelial Sodium Channel (ENaC) in Rat Kidney, Lung and Distal Colon in Response to Aldosterone.

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 724-724
Author(s):  
Shyama M E Masilamani ◽  
Gheun-Ho Kim ◽  
Mark A Knepper
Keyword(s):  
Sodium Channel ◽  
Epithelial Sodium Channel ◽  
Distal Colon ◽  
Β Subunit ◽  
Dietary Salt ◽  
Α Subunit ◽  
Salt Restriction ◽  
Γ Subunit ◽  
Dietary Salt Restriction ◽  
Epithelial Sodium Channel Enac

P170 The mineralocorticoid hormone, aldosterone increases renal tubule Na absorption via increases in the protein abundances of the α-subunit of the epithelial sodium channel (ENaC) and the 70 kDa form of the γ- subunit of ENaC (JCI 104:R19-R23). This study assesses the affect of dietary salt restriction on the regulation of the epithelial sodium channel (ENaC) in the lung and distal colon, in addition to kidney, using semiquantitative immunoblotting. Rats were placed initially on either a control Na intake (0.02 meq/day), or a low Na intake (0.2 meq/day) for 10 days. The low salt treated rats demonstrated an increase in plasma aldosterone levels at day 10 (control = 0.78 + 0.32 nM; Na restricted = 3.50 + 1.30 nM). In kidney homogenates, there were marked increases in the band density of the α-subunit of ENaC (286 % of control) and the 70 kDa form of γ-subunit of ENaC (262 % of control), but no increase in the abundance of the β-subunit of ENaC. In lung homogenates, there was no significant change in the band densities of the α, β, or γ subunits of ENaC. In distal colon, there was an increase in the band density of the β-subunit of ENaC (311 % of control) and an increase in both the 85 kDa (2355% of control) and 70 kDa (843 % of control) form of the γ subunit of ENaC in response to dietary Na restriction. However, there was no significant difference in the band density of the α-subunit of ENaC. These findings demonstrate tissue specific regulation of the three subunits of ENaC in response to dietary salt restriction.

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