Atrial Natriuretic Peptide
Also known as: ANP, ANF, atrial natriuretic factor, carperitide, atriopeptin, auriculin, cardionatrin, NPPA peptide (human gene product)
Endogenous cardiac peptide hormone — 28-amino-acid natriuretic peptide; natriuretic/diuretic agent and cardiovascular regulator
What it is
Your heart does more than pump blood — it releases a hormone called ANP that tells the kidneys to flush out excess salt and water, relaxes blood vessels, and keeps blood pressure in check. When your heart senses it is being stretched by too much fluid, ANP is the signal it sends to restore balance.
The scientific side
atrial natriuretic peptide (ANP) is a 28-amino-acid hormone synthesized and stored in atrial cardiomyocytes as a larger precursor (pre-proANP), which is processed by the protease corin to yield the biologically active mature peptide. The primary trigger for ANP secretion is mechanical stretch of the atrial wall caused by elevated intracardiac filling pressure or volume overload — a feedback signal that positions the heart as a genuine endocrine organ. Once released into the circulation, ANP binds principally to natriuretic peptide receptor type A (NPR-A), a membrane-bound guanylyl cyclase expressed in vascular smooth muscle, kidney, adrenal glands, and adipose tissue. Receptor activation catalyzes the conversion of GTP to cyclic GMP (cGMP), which in turn activates protein kinase G (PKG) and downstream effectors. The cardinal physiological actions of ANP are natriuresis (increased urinary sodium excretion through inhibition of apical sodium channels and sodium transporters in the renal nephron), diuresis (increased urine flow), and vasodilation (relaxation of vascular smooth muscle through cGMP-mediated reduction in intracellular calcium). ANP also directly antagonizes the renin-angiotensin-aldosterone system (RAAS): it suppresses renin secretion from juxtaglomerular cells, inhibits aldosterone synthesis and release from the adrenal cortex, and counteracts the vasoconstrictive and sodium-retaining effects of angiotensin II and antidiuretic hormone. A third clearance receptor, NPR-C, removes ANP from circulation through receptor-mediated internalization and degradation, contributing to ANP's short plasma half-life of approximately 2 to 3 minutes and high total-body clearance. Beyond cardiovascular regulation, research has revealed pleiotropic metabolic actions: ANP stimulates lipolysis and lipid oxidation in adipose tissue, promotes adipocyte browning, acutely lowers circulating leptin levels, and appears to improve insulin sensitivity. In endothelial cells, ANP activates autophagy via the NPR-A/PKG pathway, mediating cytoprotective responses to salt stress and inflammatory stimuli. Reduced ANP signaling has been associated with obesity, hypertension, and elevated cardiometabolic risk in genetic studies.
Class: Endogenous cardiac peptide hormone — 28-amino-acid natriuretic peptide; natriuretic/diuretic agent and cardiovascular regulator
Administration & storage
- Administration
- Intravenous continuous infusion only — the sole viable route given ANP's short half-life of approximately 2–3 minutesAdministered via controlled infusion pump in hospital or clinical research settingsBolus IV administration used in some research protocols for pharmacokinetic characterizationNo approved subcutaneousintramuscularor oral formulations of native ANP exist
- Storage
- Research-grade ANP peptides: store lyophilized powder at -20°C, protected from moisture and light; reconstituted solutions are typically used immediately. Carperitide (Japan): store per manufacturer guidelines, generally at 2–8°C before reconstitution. No stability data available for extended storage of reconstituted ANP solutions.
- Cautions
- Hypotension: ANP's vasodilatory and natriuretic actions can cause significant blood pressure reduction, particularly in patients who are hypovolemic or volume-depleted. Blood pressure monitoring during IV infusion is essential (PMIDs: 8448971, 33530911).,Hypotension risk amplified by concomitant diuretics, vasodilators, or antihypertensive agents; dose reduction or cessation may be required.,Electrolyte imbalance: ANP-induced natriuresis and diuresis can lead to sodium and potassium depletion with prolonged infusion; electrolyte monitoring is required.,Renal function: While ANP is renoprotective at physiological levels, excessive natriuresis may affect renal perfusion; monitor renal function during infusion.,Short half-life makes dosing unpredictable without continuous infusion; abrupt cessation of infusion results in rapid loss of effect.,No safety data for oral, subcutaneous, or intramuscular use; these routes are not established for native ANP.
Legal & regulatory status
Not approved by the FDA as a therapeutic agent. ANP (carperitide) itself has no FDA-approved indication. Nesiritide (recombinant BNP, a related natriuretic peptide) is the FDA-approved natriuretic peptide therapy for…
Atrial natriuretic peptide is not currently listed as a prohibited substance on the WADA Prohibited List. As an endogenous hormone, ANP itself is not classified under any prohibited section. However, synthetic ANP…
ANP (carperitide) is not approved by Health Canada as a therapeutic agent. Plasma natriuretic peptide measurements (ANP, BNP, NT-proBNP) are used in Canadian clinical practice as biomarkers for heart failure diagnosis,…
What it's studied for
- Acute decompensated heart failure treatment — carperitide (recombinant human ANP) IV infusion, Japan Prospective Cohort / Registry (large multicentre; Japan-approved drug)
- Biomarker for heart failure diagnosis, severity staging, and prognosis Established Clinical Biomarker Use / Multiple Cohort Studies
- Intravenous ANP infusion for hypertension and congestive heart failure — clinical pharmacological studies Early Clinical Pharmacology / Phase I–II
- Cardiometabolic disease — ANP-based therapeutics for hypertension and metabolic syndrome (investigational) Translational / Phase I–II (analog MANP)
- Atrial fibrillation — MR-proANP as a biomarker for stroke and AF burden Observational / Epidemiological
- Metabolic effects — ANP-mediated lipolysis, leptin suppression, and adipose tissue biology Phase I Controlled Clinical Trial
- Endothelial cytoprotection — ANP-mediated autophagy activation Preclinical / In Vitro (human cell model)
Safety signals
- Hypotension — dose-dependent blood pressure reduction
- Electrolyte disturbances — hyponatremia and hypokalemia from natriuresis and diuresis
- Renal function changes — paradoxical risk of reduced renal perfusion at high doses or in volume-depleted states
- Short half-life and rapid clearance — practical therapeutic limitation with risk of rebound effects
- Metabolic effects — leptin suppression and lipolysis activation
- Reduced ANP signaling as a risk state — low endogenous ANP associated with obesity, hypertension, and cardiometabolic disease
- Tachyphylaxis and receptor downregulation with prolonged exposure
Contraindications
About these dose ranges
Dose ranges below reflect commonly reported community protocols. Where published research cites a specific dose, the PMID is linked. Doses without citations are not clinical recommendations — they reflect what practitioners and researchers commonly report using.
Community-reported dosing
| Route | Dose | Frequency / Duration | Population / context | Source tier |
|---|---|---|---|---|
| Unspecified | Very low dose: <0.02 µg/kg/min IV; Low dose: ≥0.02 µg/kg/min IV (median ~0.025 µg/kg/min) | — | Adults with acute decompensated heart failure (Japanese clinical practice — carperitide) | Research |
| Unspecified | Standard pharmacological infusion doses (specific µg/kg dose per DRKS00024559 protocol; not fully reported in abstract) | — | Healthy adult men — ANP metabolic/hormonal study (IV bolus/infusion) | Research |
| Unspecified | IV infusions typically at 0.01–0.1 µg/kg/min in historical studies; exact doses varied by protocol | — | Hypertension / heart failure (historical clinical pharmacology studies) | Research |
| intravenous continuous infusion | Low-dose carperitide: ≥0.02 µg/kg/min IV (median 0.025 µg/kg/min in registry data) | continuous infusion during acute hospitalization | adults with acute decompensated heart failure (Japanese clinical practice; carperitide) |
No peer-reviewed studies indexed for this peptide yet.