[6] The main function of ANP is causing a reduction in expanded extracellular fluid (ECF) volume by increasing renal sodium excretion.

Reduction of blood volume by ANP can result in secondary effects such as reduction of extracellular fluid (ECF) volume, improved cardiac ejection fraction with resultant improved organ perfusion, decreased blood pressure, and increased serum potassium.

Brain natriuretic peptide (BNP) – a misnomer; it is secreted by cardiac muscle cells in the heart ventricles – is similar to ANP in its effect.

Fetal expression of NPPA is associated with the formation of chamber myocardium, muscle cells of the atria and ventricles in the early developing heart.

[10] NPPA variants affect plasma ANP concentrations, blood pressure levels, and cardiovascular diseases such as atrial fibrillation (AF).

[11] ANP-deficient mice were found to have a large increase in heart and left ventricular weight in response to volume overload, which is normally prevented by proper regulation of blood pressure.

[16] ANP is synthesized as an inactive preprohormone, encoded by the human NPPA gene located on the short arm of chromosome 1.

They are all cell surface receptors and designated: NPR-A and NPR-B have a single membrane-spanning segment with an extracellular domain that binds the ligand.

As a consequence, cGMP activates a cGMP-dependent kinase (PKG or cGK) that phosphorylates proteins at specific serine and threonine residues.

In the medullary collecting duct, the cGMP generated in response to ANP may act not only through PKG but also via direct modulation of ion channels.

Receptor-agonist binding causes the increase in renal sodium excretion, which results in a decreased ECF and blood volume.

Relaxes vascular smooth muscle in arterioles and venules by: Promotes uterine spiral artery remodeling, which is important for preventing pregnancy-induced hypertension.

[31][32][33][34] A specific ANP precursor called mid-regional pro-atrial natriuretic peptide (MRproANP) is a highly sensitive biomarker in heart failure.

[37] While this molecule has been shown to successfully restore some hemodynamic parameters following heart failure, and yield clinical improvement for kidney injury, whether it ultimately reduces mortality and its long-term effects are unknown.

[39] Preliminary research on one of such molecules, ularitide, has shown that this drug is safe, well tolerated, and effective in the treatment of acute heart failure.

[42] Omapatrilat (dual inhibitor of NEP and angiotensin-converting enzyme) developed by BMS did not receive FDA approval due to angioedema safety concerns.