ANP

ANP, or atrial natriuretic peptide, is a peptide hormone produced primarily by atrial cardiomyocytes in humans. It is encoded as a larger precursor, pro-ANP, by the NPPA gene and proteolytically processed to the mature 28‑amino‑acid peptide that is secreted into the circulation. ANP is released in response to atrial stretch from increased blood volume or pressure, and its levels rise in conditions such as fluid overload or congestive heart failure.

In target tissues, ANP binds to natriuretic peptide receptor-A (NPR-A, NPR1), which has intrinsic guanylyl cyclase activity. Receptor activation raises intracellular cyclic GMP, triggering vasodilation and changes in renal function that favor sodium excretion and water loss.

Renal effects include increased glomerular filtration rate, natriuresis, and diuresis, along with inhibition of renin release and aldosterone secretion, leading to reduced sodium reabsorption in the collecting ducts. Systemic effects include vasodilation and lowered blood pressure, which help decrease atrial pressure and circulating volume.

Physiologically, ANP contributes to short- and long-term regulation of fluid balance and blood pressure. Clinically, circulating ANP levels are studied as a biomarker in research and can be elevated in heart failure. Its actions complement other natriuretic peptides, notably BNP, and are a target of some heart failure therapies. Neprilysin degrades natriuretic peptides; inhibitors that increase ANP levels, such as in combination therapy with angiotensin receptor blockers, are used to treat heart failure with reduced ejection fraction.