Increased renal ENaC subunits and sodium retention in rats with chronic heart failure

Hong Zheng, Xuefei Liu, U. S. Rao, Kaushik P Patel

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Renal tubular dysfunction could be involved in the increased sodium and water reabsorption in chronic heart failure (CHF). The goal of the present study was to examine the molecular basis for the increased renal sodium and water retention in CHF. We hypothesized that dysregulation of renal epithelial sodium channels (ENaC) could be involved in the pathogenesis of CHF. The left coronary ligation-induced model of heart failure in the rat was used. Real-time PCR and Western blot analysis indicated that the mRNA and protein abundance of α-, (β-, and γ-infunits of ENaC were significantly increased by in the cortex (mRNA: α-ENaC Δ104 ± 24%, (β-ENaC Δ47 ± 16%, γ-ENaC Δ55 ± 18%; protein: α-ENaC Δ114 ± 28%, (β-ENaC Δ150 ± 31%, γ-ENaC Δ39 ± 5% compared with sham rats) and outer medulla (mRNA: α-ENaC Δ52 ± 18%, (β-ENaC Δ38 ± 8%, γ-ENaC Δ39 ± 13%; protein: α-ENaC Δ88 ± 16%, (β-ENaC Δ94 ± 28%, γ-ENaC Δ45 ± 9% compared with sham rats) of CHF compared with sham-operated rats. Immunohistochemistry microscopy confirmed the increased labeling of α-, (β-, and γ-ENaC infunits in the collecting duct segments in rats with CHF. Furthermore, there was a significant increase in diuretic (7-fold compared with sham) and natriuretic responses (3-fold compared with sham) to ENaC inhibitor benzamil in the rats with CHF. Absence of renal nerves produced a greater contribution of ENaC in sodium retention in rats with CHF. These results suggest that the increased expression of renal ENaC infunits may contribute to the renal sodium and water retention observed during CHF.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Renal Physiology
Volume300
Issue number3
DOIs
StatePublished - Mar 1 2011

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Heart Failure
Sodium
Kidney
Messenger RNA
Water
Epithelial Sodium Channels
Proteins
Diuretics
Ligation
Real-Time Polymerase Chain Reaction
Microscopy
Western Blotting
Immunohistochemistry

Keywords

  • Renal function
  • Sodium and water retention

ASJC Scopus subject areas

  • Physiology
  • Urology

Cite this

Increased renal ENaC subunits and sodium retention in rats with chronic heart failure. / Zheng, Hong; Liu, Xuefei; Rao, U. S.; Patel, Kaushik P.

In: American Journal of Physiology - Renal Physiology, Vol. 300, No. 3, 01.03.2011.

Research output: Contribution to journalArticle

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abstract = "Renal tubular dysfunction could be involved in the increased sodium and water reabsorption in chronic heart failure (CHF). The goal of the present study was to examine the molecular basis for the increased renal sodium and water retention in CHF. We hypothesized that dysregulation of renal epithelial sodium channels (ENaC) could be involved in the pathogenesis of CHF. The left coronary ligation-induced model of heart failure in the rat was used. Real-time PCR and Western blot analysis indicated that the mRNA and protein abundance of α-, (β-, and γ-infunits of ENaC were significantly increased by in the cortex (mRNA: α-ENaC Δ104 ± 24{\%}, (β-ENaC Δ47 ± 16{\%}, γ-ENaC Δ55 ± 18{\%}; protein: α-ENaC Δ114 ± 28{\%}, (β-ENaC Δ150 ± 31{\%}, γ-ENaC Δ39 ± 5{\%} compared with sham rats) and outer medulla (mRNA: α-ENaC Δ52 ± 18{\%}, (β-ENaC Δ38 ± 8{\%}, γ-ENaC Δ39 ± 13{\%}; protein: α-ENaC Δ88 ± 16{\%}, (β-ENaC Δ94 ± 28{\%}, γ-ENaC Δ45 ± 9{\%} compared with sham rats) of CHF compared with sham-operated rats. Immunohistochemistry microscopy confirmed the increased labeling of α-, (β-, and γ-ENaC infunits in the collecting duct segments in rats with CHF. Furthermore, there was a significant increase in diuretic (7-fold compared with sham) and natriuretic responses (3-fold compared with sham) to ENaC inhibitor benzamil in the rats with CHF. Absence of renal nerves produced a greater contribution of ENaC in sodium retention in rats with CHF. These results suggest that the increased expression of renal ENaC infunits may contribute to the renal sodium and water retention observed during CHF.",
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AB - Renal tubular dysfunction could be involved in the increased sodium and water reabsorption in chronic heart failure (CHF). The goal of the present study was to examine the molecular basis for the increased renal sodium and water retention in CHF. We hypothesized that dysregulation of renal epithelial sodium channels (ENaC) could be involved in the pathogenesis of CHF. The left coronary ligation-induced model of heart failure in the rat was used. Real-time PCR and Western blot analysis indicated that the mRNA and protein abundance of α-, (β-, and γ-infunits of ENaC were significantly increased by in the cortex (mRNA: α-ENaC Δ104 ± 24%, (β-ENaC Δ47 ± 16%, γ-ENaC Δ55 ± 18%; protein: α-ENaC Δ114 ± 28%, (β-ENaC Δ150 ± 31%, γ-ENaC Δ39 ± 5% compared with sham rats) and outer medulla (mRNA: α-ENaC Δ52 ± 18%, (β-ENaC Δ38 ± 8%, γ-ENaC Δ39 ± 13%; protein: α-ENaC Δ88 ± 16%, (β-ENaC Δ94 ± 28%, γ-ENaC Δ45 ± 9% compared with sham rats) of CHF compared with sham-operated rats. Immunohistochemistry microscopy confirmed the increased labeling of α-, (β-, and γ-ENaC infunits in the collecting duct segments in rats with CHF. Furthermore, there was a significant increase in diuretic (7-fold compared with sham) and natriuretic responses (3-fold compared with sham) to ENaC inhibitor benzamil in the rats with CHF. Absence of renal nerves produced a greater contribution of ENaC in sodium retention in rats with CHF. These results suggest that the increased expression of renal ENaC infunits may contribute to the renal sodium and water retention observed during CHF.

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