Salt and gene expression: evidence for [Na+]i/[K+]i-mediated signaling pathways.

Abstract

Our review focuses on the recent data showing that gene transcription and translation are under the control of signaling pathways triggered by modulation of the intracellular sodium/potassium ratio ([Na+]i/[K+]i). Side-by-side with sensing of osmolality elevation by tonicity enhancer-binding protein (TonEBP, NFAT5), [Na+]i/[K+]i-mediated excitation-transcription coupling may contribute to the transcriptomic changes evoked by high salt consumption. This novel mechanism includes the sensing of heightened Na+ concentration in the plasma, interstitial, and cerebrospinal fluids via augmented Na+ influx in the endothelium, immune system cells, and the subfornical organ, respectively. In these cells, [Na+]i/[K+]i ratio elevation, triggered by augmented Na+ influx, is further potentiated by increased production of endogenous Na+,K+-ATPase inhibitors documented in salt-sensitive hypertension.

• Authors: Sergei N Orlov, Pavel Hamet
• Journal: Pflugers Archiv : European journal of physiology (Pflugers Arch) Vol. 467 Issue 3 Pg. 489-98 (Mar 2015) ISSN: 1432-2013 [Electronic] Germany
• PMID: 25479826 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Sodium Channels
• Sodium
• Sodium-Potassium-Exchanging ATPase
• Potassium

Topics

• Animals
• Humans
• Immune System (metabolism)
• Potassium (metabolism)
• Signal Transduction
• Sodium (metabolism)
• Sodium Channels (genetics, metabolism)
• Sodium-Potassium-Exchanging ATPase (genetics, metabolism)
• Subfornical Organ (metabolism)
• Transcriptional Activation