PeptideHormone

Atrial natriuretic peptideANP

Released when the atria stretch; promotes salt and water excretion.

EndogenousEstablished

Identity

Class
Natriuretic peptide (28 aa, ring-structured)
Source
Atrial cardiomyocytes
Receptor
Natriuretic peptide receptor A (NPR-A, a guanylyl cyclase)

Key properties

Molecular weight
~3,080.5 Da
Half-life (native)
~2–3 min
Model dosing

Approximate values for the native hormone. Engineered analogs are often deliberately larger and far longer-acting.

Mechanism

Atrial stretch from volume overload releases ANP, which binds NPR-A to raise cGMP, promoting sodium and water excretion and vasodilation — reducing the blood volume and pressure that triggered it. It is a direct negative-feedback brake on cardiac load.

Reference notes

  • ANP signals through a membrane guanylyl-cyclase receptor (cGMP), not a GPCR — a different second-messenger system from most of this catalog.
  • Its trigger is mechanical: atrial wall stretch.
  • It opposes the renin-angiotensin system's salt-and-water retention.

Selected literature

Curated peer-reviewed reviews, sourced from PubMed. Selected for relevance, not exhaustive — open any entry on PubMed for the full record and its primary citations.

  1. 1.Atrial Natriuretic Peptide: Structure, Function, and Physiological Effects: A Narrative Review · Current cardiology reviews, 2021 · PMID 33530911
  2. 2.Cardiac natriuretic peptides · Nature reviews. Cardiology, 2020 · PMID 32444692