Dietary salt sensing in the brain, kidney, and gastrointestinal tract involves specific cell types, osmolality changes, and distinct molecular and electrochemical mechanisms.
Excess dietary salt (NaCl) intake is strongly correlated with cardiovascular disease and is a major contributing factor to the pathogenesis of hypertension. NaCl-sensitive hypertension is a multisystem disorder that involves renal dysfunction, vascular abnormalities, and neurogenically-mediated increases in peripheral resistance. Despite a major research focus on organ systems and these effector mechanisms causing NaCl-induced increases in arterial blood pressure, relatively less research has been directed at elucidating how NaCl is sensed by various tissues to elicit these downstream effects. The purpose of this review is to discuss how the brain, kidney, and gastrointestinal tract sense NaCl including key cell types, the role of NaCl versus osmolality, and the underlying molecular and electrochemical mechanisms.
Stocker et al. (Wed,) conducted a review in Hypertension. Dietary salt (NaCl) was evaluated. Dietary salt sensing in the brain, kidney, and gastrointestinal tract involves specific cell types, osmolality changes, and distinct molecular and electrochemical mechanisms.