Figure 1.

Sodium balance. An adequate extracellular concentration of Na⁺ ([Na⁺]_ext) is vital for the functioning of our cells. Diet provides the daily amount of Na⁺ to balance off losses through kidney, intestine, and sweating (not shown). Food Na⁺ is detected mainly by taste buds, which contained sensory cells able to sense this cation through sodium receptors (ENaC and others not yet identified). Taste information is fundamental for recognizing the quality and the intensity of saltiness. However, large salt concentration may also activate trigeminal nerve endings, which contain another “salt” receptor (TRPV1). This sensory pathway is believed to provide information on stimulus intensity in supra-threshold salt concentration range. Chemosensory signals are processed in the brain for conscious perception and for sodium appetite regulation. The outcome of central processing guides salt intake (Na⁺ input). Note that oral chemosensory input provides feed-forward signals alerting central neurons on the presence of sodium-containing foods before Na⁺ absorption has occurred in the gut. Once absorbed, ingested Na⁺ is confined mainly to the extracellular space, and changes in its extracellular concentration affect blood volume and blood pressure, which in turn influence the renin-angiotensin-aldosterone system (RAAS). RAAS controls the amount of Na⁺ lost by kidney and colon (Na⁺ output), and also provides feedback to neural centers and taste buds to regulate sodium appetite and salt sensitivity, respectively. In turn, the brain modulates renin secretion through baroreceptor reflexes. Papers in this Special Issue touch upon some of the processes (Na⁺ detection, eating behavior, blood pressure regulation, Na⁺ output regulation) that are associated with the handling of food Na⁺ by our body. Note that, for simplicity, other factors involved in sodium balance, such as the atrial natriuretic peptide, are not shown.