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Natriuretic peptide A (NPPA), also known as atrial natriuretic peptide (ANP), is a peptide hormone predominantly produced by cardiac atrial myocytes. It plays a central role in cardiovascular and renal homeostasis by promoting vasodilation, natriuresis, and diuresis, and by inhibiting aldosterone secretion and cardiac hypertrophy. NPPA is processed from a larger precursor, preproANP, and acts primarily through the natriuretic peptide receptor A (NPR-A), leading to the production of cyclic GMP which mediates its biological actions. NPPA is elevated in heart failure and cardiac stress, serving as a key diagnostic and prognostic biomarker. Therapeutically, NPPA and its analogs have been developed for managing acute decompensated heart failure, though clinical use is tempered by concerns of hypotension and variable efficacy. NPPA's modulation of blood volume, vascular tone, and cardiac remodeling underlies its designation as both a physiological regulator and a therapeutic target in cardiovascular disease[1][3][7].
Agonists (recombinant/analogous peptides): Direct activation of natriuretic peptide receptor A (NPR-A), leading to cGMP production, resulting in vasodilation, natriuresis, diuresis, and inhibition of cardiac hypertrophy[1][3][6]. Neprilysin inhibitors: Prevent degradation of endogenous natriuretic peptides, increasing their biological activity[2][3].
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