ANP (Atrial Natriuretic Peptide)
ANP is a 28-aa cardiac peptide secreted by atria in response to volume/pressure overload. It activates NPR-A receptors to increase renal sodium and water excretion, reduce blood pressure, and inhibit renin-aldosterone. Key cardiovascular research tool.
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Compound Profile
ANP (Atrial Natriuretic Peptide)
Key Data
Research reference only
Research Focus
Preclinical data
⚠ Research & Educational Use Only. ANP (Atrial Natriuretic Peptide) is a research chemical documented here for scientific education. All information references peer-reviewed literature and preclinical/clinical study data. Not for human consumption. Not medical advice. Consult a licensed researcher or healthcare professional before any laboratory use.
- Potent natriuresis and diuresis via NPR-A (cGMP-coupled) receptors in renal collecting duct
- Reduces blood pressure via vasodilation and inhibition of the renin-angiotensin-aldosterone system (RAAS)
- Suppresses aldosterone secretion from adrenal cortex — reduces sodium retention
- ANP (Atrial Natriuretic Peptide) is not FDA-approved for human use. It is a research chemical for scientific study only.
Research At a Glance
- Potent natriuresis and diuresis via NPR-A (cGMP-coupled) receptors in renal collecting duct
- Reduces blood pressure via vasodilation and inhibition of the renin-angiotensin-aldosterone system (RAAS)
- Suppresses aldosterone secretion from adrenal cortex — reduces sodium retention
- Inhibits sympathetic nervous system activity — reduces heart rate and cardiac output
In Plain English
Simple summaryANP (atrial natriuretic peptide) is a 28-amino acid cyclic peptide your heart's atria release when they detect elevated blood pressure or increased blood volume. It's the heart's own antihypertensive signal: ANP tells the kidneys to excrete more sodium and water (natriuresis and diuresis), relaxes blood vessels, and suppresses the renin-angiotensin-aldosterone system -- all actions that reduce blood pressure and circulating blood volume. Nesiritide (synthetic BNP, brain natriuretic peptide) is a related peptide drug approved for acute heart failure decompensation. ANP itself and its analogues have been studied in acute heart failure, hypertension, and cardiac remodeling, but the short half-life (minutes) has limited standalone therapeutic use.
- Potent natriuresis and diuresis via NPR-A (cGMP-coupled) receptors in renal collecting duct
- Reduces blood pressure via vasodilation and inhibition of the renin-angiotensin-aldosterone system (RAAS)
- Suppresses aldosterone secretion from adrenal cortex — reduces sodium retention
The full scientific detail, mechanisms, citations, and dosing data, follows below.
What is ANP (Atrial Natriuretic Peptide)?
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Atrial Natriuretic Peptide (ANP, also called atrial natriuretic factor, ANF) is a 28-amino acid peptide cardiac hormone secreted primarily by cardiac atrial cardiomyocytes in response to mechanical stretch caused by elevated atrial pressure and volume. It was discovered in 1981 by de Bold et al., who demonstrated that intravenous injection of atrial extracts in rats produced dramatic natriuresis — a finding that revealed the heart as an endocrine organ.
ANP is synthesized as a 151-amino acid precursor (pre-pro-ANP), stored in secretory granules in atrial cardiomyocytes as pro-ANP (108 amino acids), and cleaved to active ANP (28 amino acids) plus N-terminal pro-ANP upon secretion.
**Signaling mechanisms:** ANP binds NPR-A (Natriuretic Peptide Receptor A, also called GC-A), a receptor guanylyl cyclase, to generate intracellular cGMP. cGMP activates PKG (protein kinase G), which produces: 1. **Renal effects**: Increases glomerular filtration rate (afferent arteriole dilation, efferent arteriole constriction), inhibits Na+ reabsorption in the inner medullary collecting duct → natriuresis and diuresis 2. **Vascular effects**: Smooth muscle relaxation via PKG-mediated MLCK inhibition → vasodilation 3. **Adrenal effects**: Inhibits aldosterone synthesis and secretion from zona glomerulosa → further reduces sodium retention 4. **Cardiac effects**: Inhibits cardiac fibroblast proliferation and collagen production → anti-fibrotic (via cGMP/PKG) 5. **Sympathetic inhibition**: Reduces renin secretion and sympathetic nervous system activity centrally
**The natriuretic peptide family:** ANP (from atria) is the founding member. BNP (brain/B-type natriuretic peptide) is secreted primarily by ventricular cardiomyocytes under increased wall stress and is the basis for cardiac biomarkers NT-proBNP and BNP (elevated in heart failure). CNP (C-type natriuretic peptide) acts via NPR-B and has bone-anabolic and vascular smooth muscle effects.
ANP plasma levels are elevated in hypertension, heart failure, and renal disease, and serve as biomarkers of cardiac volume status. Research applications span heart failure physiology, kidney disease, cardiac fibrosis, pulmonary hypertension, and the RAAS counterregulation axis.
By the Numbers
Key Research Benefits
Documented effects observed in preclinical and clinical studies on ANP (Atrial Natriuretic Peptide). See all Healing & Recovery peptides for comparison.
Side Effects & Risks
Adverse effects reported in the research literature. All data sourced from preclinical and clinical study reports. View all peptides' side effects →
Dosing Data from the Literature
Doses referenced below are sourced from published preclinical and clinical studies. Use the peptide dose calculator to convert these values to injection volume.
ANP human research protocols:
IV infusion: 0.1-0.2 mcg/kg/min for volume overload and heart failure studies Nesiritide (recombinant BNP, structurally related): 2 mcg/kg IV bolus then 0.01 mcg/kg/min infusion — was FDA-approved for acute decompensated heart failure (withdrawn due to renal concerns)
Research applications: Renal physiology (ANP-induced natriuresis studies), cardiac fibrosis (cGMP pathway), heart failure biomarker research
Administration in Research Settings
Standard reconstitution and administration methodology for laboratory research use.
ANP is an IV research peptide due to its <3-minute half-life. Continuous infusion is required for sustained effects. Not suitable for SC administration. For research, dilute in 0.9% NaCl with 0.1% BSA to prevent adsorption.
What the research doesn't show
ANP's very short half-life (2-3 minutes in plasma) makes it impractical as a standalone drug. Nesiritide (synthetic BNP) made it to FDA approval for acute heart failure but its clinical value has been debated -- studies showed it reduces symptoms but didn't improve mortality. The natriuretic peptide system is well-understood mechanistically but hasn't translated into a transformative therapeutic class despite decades of drug development.
Medical Expert Videos
Physicians, researchers, and pharmacologists explain ANP (Atrial Natriuretic Peptide), covering mechanisms of action, clinical context, and study findings.
Videos sourced from YouTube search. KnowYourPeptide does not endorse any individual creator. For research education only.
The Bottom Line
ANP (Atrial Natriuretic Peptide) has a growing body of preclinical evidence and a well-characterised safety profile in research settings. The most-studied application is: potent natriuresis and diuresis via npr-a (cgmp-coupled) receptors in renal collecting duct.
The most commonly reported side effect in research subjects is hypotension — rapid fall in blood pressure with iv administration. It is a research chemical, not approved for human use.
Frequently Asked Questions
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Quick Reference
How It Compares
BNP (B-type natriuretic peptide) is released from the ventricles rather than atria and has the same mechanism -- nesiritide is synthetic BNP and is FDA-approved for acute decompensated heart failure. CNP (C-type natriuretic peptide) is produced locally in the vasculature. Bradykinin has overlapping vasodilatory effects. BNP measurement is the clinical biomarker for heart failure severity; ANP is less commonly measured clinically but equally fundamental to natriuretic peptide biology.
Compare ANP (Atrial Natriuretic Peptide) side-by-sideResearch Use Only
This information is for educational research purposes only. This is not medical advice. Consult a qualified healthcare professional.