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See related article, pp 927–933Hypertension is one of the most prevalent multifactorial cardiovascular disorders caused by both genetic and environmental factors. Overwhelming evidence shows that abnormal sodium regulation because of either hereditary factors or overconsumption of salt may lead to salt-sensitive hypertension.1,2 Sodium regulation is complex mainly because of its dependence on neuronal, hormonal, and local factors.1,2 Hormonal regulation involves a complex array of both natriuretic and antinatriuretic hormones affecting renal sodium reabsorption.1,2 During normal sodium intake, antinatriuretic hormones predominate whereby renin–angiotensin–aldosterone system maintains positive sodium balance by increasing renal sodium absorption mainly because of the activation of tubular sodium transporters.1,2 However, under sodium replete conditions, natriuretic factors, such as dopamine, nitric oxide, and arterial natriuretic peptide, inhibit renal tubular sodium transporters, leading to increased sodium excretion.1,2 The kidney, especially the renal proximal tubule, which is responsible for ≈60% of total renal sodium reabsorption, is critical in the regulation of sodium balance.1,2 Reports from our laboratory and others have shown that dopamine produced by the kidney is critically involved in the excretion of an Na+ load.3,4 Dopamine, via D1-like (composed of D1 receptor [D1R] and D5 receptor subtypes) and D2-like receptors (composed of D2 receptor, D3 receptor, and D4 receptor subtypes), increases sodium excretion secondary to a decrease in the activity …

Novel Gastro-Renal Axis and Sodium Regulation During Hypertension