natriuretic

Natriuretic describes agents or phenomena that promote natriuresis, the excretion of sodium in the urine. In physiology, the term is most closely associated with natriuretic peptides, a family of hormones that regulate fluid and electrolyte balance and influence blood pressure.

The principal natriuretic peptides are atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP). ANP is primarily produced in the atria, BNP in the ventricles, and CNP in endothelial and other tissues. Their release is stimulated by increased cardiac wall stretch, myocardial volume overload, or other stressors. These peptides exert their effects by binding to natriuretic peptide receptors (NPR-A and NPR-B) that possess guanylyl cyclase activity, leading to elevated cyclic GMP levels. This signaling promotes vasodilation, increases glomerular filtration rate, inhibits renin and aldosterone secretion, and directly reduces sodium reabsorption in the renal collecting ducts, resulting in natriuresis and diuresis.

Clinically, elevated levels of BNP and its inactive fragment NT-proBNP are used as biomarkers for heart failure and volume overload. Therapies that augment natriuretic peptide signaling, such as neprilysin inhibitors (often combined with angiotensin receptor blockers), aim to enhance these natriuretic effects to improve symptoms and outcomes in heart failure. The natriuretic system is influenced by age, renal function, and comorbidities, and its interpretation requires context within overall cardiovascular status.