scholarly journals Sub-chronic testosterone treatment increases the levels of epithelial sodium channel (ENaC)-α,βandγin the kidney of orchidectomized adult male Sprague–Dawley rats

PeerJ ◽  
2016 ◽  
Vol 4 ◽  
pp. e2145 ◽  
Author(s):  
Su Yi Loh ◽  
Nelli Giribabu ◽  
Naguib Salleh
Keyword(s):  
Blood Pressure ◽  
Sodium Channel ◽  
Adult Male ◽  
Epithelial Sodium Channel ◽  
Physiological Parameter ◽  
Mrna Levels ◽  
Sprague Dawley ◽  
Collecting Ducts ◽  
Distal Tubules ◽  
Epithelial Sodium Channel Enac

Testosterone has been reported to cause blood pressure to increase. However mechanisms that underlie the effect of this hormone on this physiological parameter are currently not well understood. The aims of this study were to investigate effects of testosterone on expression ofα,βandγ-epithelial sodium channel (ENaC) proteins and messenger RNAs (mRNAs) in kidneys, the channel known to be involved in Na+reabsorption, which subsequently can affect the blood pressure.Methods.Adult male Sprague–Dawley (SD) rats were orchidectomized fourteen days prior to receiving seven days treatment with testosterone propionate (125 µg/kg/day or 250 µg/kg/day) with or without flutamide (androgen receptor blocker) or finasteride (5α-reductase inhibitor). Following sacrifice, the kidneys were removed and were subjected forα,βandγ-ENaC protein and mRNA expression analyses by Western blotting and Real-time PCR (qPCR) respectively. The distribution ofα,βandγ-ENaC proteins in kidneys were observed by immunofluorescence.Results.Theα,βandγ-ENaC proteins and mRNA levels in kidneys were enhanced in rats which received testosterone-only treatment. In these rats,α,βandγ-ENaC proteins were distributed in the distal tubules and collecting ducts of the nephrons. Co-treatment with flutamide or finasteride resulted in the levels ofα,βandγ-ENaC proteins and mRNAs in kidneys to decrease. In conclusions, increases inα,βandγ-ENaC protein and mRNA levels in kidneys mainly in the distal tubules and collecting ducts under testosterone influence might lead to enhance Na+reabsorption which subsequently might cause an increase in blood pressure.

Regulation of blood pressure, the epithelial sodium channel (ENaC), and other key renal sodium transporters by chronic insulin infusion in rats

2006 ◽  
Vol 290 (5) ◽  
pp. F1055-F1064 ◽  
Author(s):  
Jian Song ◽  
Xinqun Hu ◽  
Shahla Riazi ◽  
Swasti Tiwari ◽  
James B. Wade ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sodium Channel ◽  
Insulin Infusion ◽  
Collecting Duct ◽  
Epithelial Sodium Channel ◽  
Kidney Cortex ◽  
Sodium Reabsorption ◽  
Cortical Collecting Duct ◽  
Sprague Dawley ◽  
Epithelial Sodium Channel Enac

Hyperinsulinemia is associated with hypertension. Dysregulation of renal distal tubule sodium reabsorption may play a role. We evaluated the regulation of the epithelial sodium channel (ENaC) and the thiazide-sensitive Na-Cl cotransporter (NCC) during chronic hyperinsulinemia in rats and correlated these changes to blood pressure as determined by radiotelemetry. Male Sprague-Dawley rats (∼270 g) underwent one of the following three treatments for 4 wk ( n = 6/group): 1) control; 2) insulin-infused plus 20% dextrose in drinking water; or 3) glucose water-drinking (20% dextrose in water). Mean arterial pressures were increased by insulin and glucose (mmHg at 3 wk): 98 ± 1 (control), 107 ± 2 (insulin), and 109 ± 3 (glucose), P < 0.01. Insulin (but not glucose) increased natriuretic response to benzamil (ENaC inhibitor) and hydrochlorothiazide (NCC inhibitor) on average by 125 and 60%, respectively, relative to control rats, suggesting increased activity of these reabsorptive pathways. Neither insulin nor glucose affected the renal protein abundances of NCC or the ENaC subunits (α, β, and γ) in kidney cortex, outer medulla, or inner medulla in a major way, as determined by immunoblotting. However, insulin and to some extent glucose increased apical localization of these subunits in cortical collecting duct principal cells, as determined by immunoperoxidase labeling. In addition, insulin decreased cortical “with no lysine” kinase (WNK4) abundance (by 16% relative to control), which may have increased NCC activity. Overall, insulin infusion increased blood pressure, and NCC and ENaC activity in rats. Increased apical targeting of ENaC and decreased WNK4 expression may be involved.

scholarly journals The sodium chloride cotransporter (NCC) and epithelial sodium channel (ENaC) associate

2016 ◽  
Vol 473 (19) ◽  
pp. 3237-3252 ◽  
Author(s):  
Abinash C. Mistry ◽  
Brandi M. Wynne ◽  
Ling Yu ◽  
Viktor Tomilin ◽  
Qiang Yue ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sodium Chloride ◽  
Sodium Channel ◽  
Epithelial Sodium Channel ◽  
Transport Proteins ◽  
Salt Transport ◽  
Native Page ◽  
Sodium Chloride Cotransporter ◽  
Direct Binding ◽  
Epithelial Sodium Channel Enac

The thiazide-sensitive sodium chloride cotransporter (NCC) and the epithelial sodium channel (ENaC) are two of the most important determinants of salt balance and thus systemic blood pressure. Abnormalities in either result in profound changes in blood pressure. There is one segment of the nephron where these two sodium transporters are coexpressed, the second part of the distal convoluted tubule. This is a key part of the aldosterone-sensitive distal nephron, the final regulator of salt handling in the kidney. Aldosterone is the key hormonal regulator for both of these proteins. Despite these shared regulators and coexpression in a key nephron segment, associations between these proteins have not been investigated. After confirming apical localization of these proteins, we demonstrated the presence of functional transport proteins and native association by blue native PAGE. Extensive coimmunoprecipitation experiments demonstrated a consistent interaction of NCC with α- and γ-ENaC. Mammalian two-hybrid studies demonstrated direct binding of NCC to ENaC subunits. Fluorescence resonance energy transfer and immunogold EM studies confirmed that these transport proteins are within appropriate proximity for direct binding. Additionally, we demonstrate that there are functional consequences of this interaction, with inhibition of NCC affecting the function of ENaC. This novel finding of an association between ENaC and NCC could alter our understanding of salt transport in the distal tubule.

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

Renin–aldosterone response, urinary Na/K ratio and growth in pseudohypoaldosteronism patients with mutations in epithelial sodium channel (ENaC) subunit genes

2008 ◽  
Vol 111 (3-5) ◽  
pp. 268-274 ◽  
Author(s):  
Aaron Hanukoglu ◽  
Oded Edelheit ◽  
Yafit Shriki ◽  
Maria Gizewska ◽  
Nathan Dascal ◽  
...  
Keyword(s):  
Sodium Channel ◽  
Epithelial Sodium Channel ◽  
Epithelial Sodium Channel Enac
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