Atrial natriuretic peptide (ANP)
Also known as: ANP, atrial natriuretic factor, BNP, B-type natriuretic peptide, NT-proBNP
A 28-amino-acid peptide released by atrial myocytes when they are stretched by increased blood volume; it lowers blood volume and pressure by promoting sodium and water excretion and vasodilation, opposing the renin–angiotensin–aldosterone system.
Overview
Atrial myocytes store ANP in secretory granules and release it in proportion to atrial wall stretch (volume expansion, high central venous pressure, tachycardia). Its sister hormone B-type (brain) natriuretic peptide (BNP) is produced mainly by ventricular myocytes in response to ventricular wall stress and is the clinically measured marker.
Both bind natriuretic peptide receptor-A, a transmembrane guanylyl cyclase that generates cGMP. Effects: (1) kidney — dilation of the afferent and constriction of the efferent arteriole (raising GFR), inhibition of Na⁺ reabsorption in the collecting duct, and inhibition of renin; (2) adrenal — inhibition of aldosterone; (3) posterior pituitary — reduced ADH; (4) vessels — vasodilation and increased capillary permeability, shifting fluid to the interstitium. The net result is natriuresis, diuresis and lower blood pressure. Natriuretic peptides are cleared by NPR-C and degraded by neprilysin (neutral endopeptidase).
- Location
Source: atrial myocytes (ANP); ventricular myocytes (BNP). Targets: kidney, adrenal cortex, vascular smooth muscle, posterior pituitary.
Function
- Natriuresis and diuresis (increased GFR, reduced collecting-duct Na⁺ reabsorption).
- Inhibition of renin, aldosterone and ADH.
- Vasodilation and reduction of blood pressure and preload.
- Physiology
Class: peptide (ANP 28 aa; BNP 32 aa). Receptor: NPR-A — guanylyl cyclase/cGMP. Half-life: ANP ≈2–3 min; BNP ≈20 min; NT-proBNP ≈1–2 h.
- Regulation
Stimulated by atrial (ANP) or ventricular (BNP) stretch, angiotensin II, endothelin and sympathetic stimulation; cleared by NPR-C and neprilysin.
Clinical significance
BNP and NT-proBNP in heart failure
Raised in heart failure in proportion to severity; a normal level makes heart failure unlikely (high negative predictive value) and guides referral for echocardiography. Also raised in renal failure, atrial fibrillation, pulmonary embolism and with age; lowered by obesity.
Neprilysin inhibition
Sacubitril/valsartan blocks breakdown of natriuretic peptides while blocking AT1 receptors and reduces mortality in heart failure with reduced ejection fraction (BNP rises on treatment, so NT-proBNP is used for monitoring).
Compiled from standard anatomy and physiology references — see the Endocrine System sources. For education only; not medical advice.