A Role of the Epithelial Sodium Channel in Human Salt Taste Transduction?

2008 ◽  
Vol 1 (1) ◽  
pp. 78-90 ◽  
Author(s):  
Frauke Stähler ◽  
Katja Riedel ◽  
Stefanie Demgensky ◽  
Katrin Neumann ◽  
Andreas Dunkel ◽  
...  
Keyword(s):  
Sodium Channel ◽  
Epithelial Sodium Channel ◽  
Salt Taste ◽  
Taste Transduction

Role of the α-, β-, and γ-Subunits of Epithelial Sodium Channel in a Model of Polygenic Hypertension

Hypertension ◽  
1997 ◽  
Vol 29 (1) ◽  
pp. 131-136 ◽  
Author(s):  
Reinhold Kreutz ◽  
Berthold Struk ◽  
Speranza Rubattu ◽  
Norbert Hübner ◽  
Josiane Szpirer ◽  
...  
Keyword(s):  
Sodium Channel ◽  
Epithelial Sodium Channel

scholarly journals Insulin activates epithelial sodium channel (ENaC) via phosphoinositide 3-kinase in mammalian taste receptor cells

2011 ◽  
Vol 300 (4) ◽  
pp. C860-C871 ◽  
Author(s):  
Arian F. Baquero ◽  
Timothy A. Gilbertson
Keyword(s):  
Sodium Channel ◽  
Taste Receptor ◽  
Epithelial Sodium Channel ◽  
Endocrine Regulation ◽  
Salt Taste ◽  
Receptor Cells ◽  
Taste Receptor Cells ◽  
Phosphoinositide 3 Kinase ◽  
20 Nm ◽  
Epithelial Sodium Channel Enac

Diabetes is a profound disease that results in a severe lack of regulation of systemic salt and water balance. From our earlier work on the endocrine regulation of salt taste at the level of the epithelial sodium channel (ENaC), we have begun to investigate the ability of insulin to alter ENaC function with patch-clamp recording on isolated mouse taste receptor cells (TRCs). In fungiform and vallate TRCs that exhibit functional ENaC currents (e.g., amiloride-sensitive Na+ influx), insulin (5–20 nM) caused a significant increase in Na+ influx at −80 mV (EC50 = 7.53 nM). The insulin-enhanced currents were inhibited by amiloride (30 μM). Similarly, in ratiometric Na+ imaging using SBFI, insulin treatment (20 nM) enhanced Na+ movement in TRCs, consistent with its action in electrophysiological assays. The ability of insulin to regulate ENaC function is dependent on the enzyme phosphoinositide 3-kinase since treatment with the inhibitor LY294002 (10 μM) abolished insulin-induced changes in ENaC. To test the role of insulin in the regulation of salt taste, we have characterized behavioral responses to NaCl using a mouse model of acute hyperinsulinemia. Insulin-treated mice show significant avoidance of NaCl at lower concentrations than the control group. Interestingly, these differences between groups were abolished when amiloride (100 μM) was added into NaCl solutions, suggesting that insulin was regulating ENaC. Our results are consistent with a role for insulin in maintaining functional expression of ENaC in mouse TRCs.

scholarly journals Role of the epithelial sodium channel in salt-sensitive hypertension

2011 ◽  
Vol 32 (6) ◽  
pp. 789-797 ◽  
Author(s):  
Yan Sun ◽  
Jia-ning Zhang ◽  
Dan Zhao ◽  
Qiu-shi Wang ◽  
Yu-chun Gu ◽  
...  
Keyword(s):  
Sodium Channel ◽  
Epithelial Sodium Channel ◽  
Salt Sensitive Hypertension

Role of SGK in hormonal regulation of epithelial sodium channel in A6 cells

2003 ◽  
Vol 284 (2) ◽  
pp. C404-C414 ◽  
Author(s):  
Diego Alvarez de la Rosa ◽  
Cecilia M. Canessa
Keyword(s):  
Sodium Channel ◽  
Hormonal Regulation ◽  
Apical Membrane ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Epithelial Sodium Channel ◽  
Hormonal Stimulation ◽  
A6 Cells ◽  
Epithelial Sodium Channel Enac

The purpose of this study was to examine the role of the serum- and glucocorticoid-induced kinase (SGK) in the activation of the epithelial sodium channel (ENaC) by aldosterone, arginine vasopressin (AVP), and insulin. We used a tetracycline-inducible system to control the expression of wild-type (SGK[Formula: see text]), constitutively active (S425D mutation; SGK[Formula: see text]), or inactive (K130M mutation; SGK[Formula: see text]) SGK in A6 cells independently of hormonal stimulation. The effect of SGK expression on ENaC activity was monitored by measuring transepithelial amiloride-sensitive short-circuit current ( I sc) of transfected A6 cell lines. Expression of SGK[Formula: see text] or SGK[Formula: see text] and aldosterone stimulation have additive effects on I sc. Although SGK could play some role in the aldosterone response, our results suggest that other mechanisms take place. SGK[Formula: see text] abrogates the responses to AVP and insulin; hence, in the signaling pathways of these hormones there is a shared step that is stimulated by SGK. Because AVP and insulin induce fusion of vesicles to the apical membrane, our results support the notion that SGK promotes incorporation of channels in the apical membrane.

scholarly journals Role of the Wrist Domain in the Response of the Epithelial Sodium Channel to External Stimuli

2012 ◽  
Vol 287 (53) ◽  
pp. 44027-44035 ◽  
Author(s):  
Shujie Shi ◽  
Marcelo D. Carattino ◽  
Thomas R. Kleyman
Keyword(s):  
Sodium Channel ◽  
Epithelial Sodium Channel ◽  
External Stimuli
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