Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (635 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A potent natriuretic and vasodilatory peptide or mixture of different-sized low molecular weight peptides derived from a common precursor and secreted mainly by the heart atrium. All these peptides share a sequence of about 20 amino acids.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: ANP; Atrial Natriuretic Peptide; Natriuretic Peptide, Atrial; Peptide, Atrial Natriuretic; Atriopeptins; ANF; Atrial Natriuretic Peptides; Peptides, Atrial Natriuretic.
Where it fits in the MeSH classification
- Broader topics
- Natriuretic Peptides
- See also
- Receptors, Atrial Natriuretic Factor
Related concepts
- Peptides
- Heart Atrium
- Amino Acids
Research landscape
PubMed indexes 15,660 records tagged with the MeSH heading “Atrial Natriuretic Factor” (counts retrieved 2026-10-31). 509 of them (3.3%) were published from 2020 onward, and the busiest period so far is through 1999 with 10,154 records.
Reviews account for 1,449 records (9.3%) and meta-analyses for 24. Randomized controlled trials number 676 (4.3%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 10,154 |
| 2000-2009 | 3,256 |
| 2010-2019 | 1,741 |
| 2020 onward | 509 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,449 | 9.3% |
| Meta-analyses | 24 | 0.2% |
| Randomized controlled trials | 676 | 4.3% |
Method: PubMed query "Atrial Natriuretic Factor"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Hypervolemia increases release of atrial natriuretic peptide and shedding of the endothelial glycocalyx | 2014 | Research article Design not recorded in structured metadata | 245 | cc by PMID 25497357 · DOI · PMC4201669 |
| Structure and function of the Nppa-Nppb cluster locus during heart development and disease | 2018 | Review article Design not recorded in structured metadata | 108 | cc by PMID 29302701 · DOI · PMC5852170 |
| Role of Cardiac Natriuretic Peptides in Heart Structure and Function | 2022 | Review article Design not recorded in structured metadata | 66 | cc by PMID 36430893 · DOI · PMC9697447 |
| Single intramuscular injection of self-amplifying RNA of Nppa to treat myocardial infarction | 2026 | Research article Design not recorded in structured metadata | 14 | cc by PMID 41785353 · DOI · PMC13124201 |
Hypervolemia increases release of atrial natriuretic peptide and shedding of the endothelial glycocalyx [1]
Abstract reading summary — source excerpts
- Opening excerpt
- IntroductionAcute normovolemic hemodilution (ANH) and volume loading (VL) are standard blood-sparing procedures.
- Closing excerpt
- This perturbation must be expected to impair the vascular barrier, implying that VL may not be as safe as generally assumed and that it should be critically evaluated.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (210 words)
IntroductionAcute normovolemic hemodilution (ANH) and volume loading (VL) are standard blood-sparing procedures. However, VL is associated with hypervolemia, which may cause tissue edema, cardiopulmonary complications and a prolonged hospital stay. The body reacts to hypervolemia with release of atrial natriuretic peptide (ANP) from the heart. ANP has been shown to deteriorate the endothelial glycocalyx, a vital part of the vascular permeability barrier. The aim of the present study was to evaluate and compare ANP release and damage to the glycocalyx during ANH and VL.MethodsANH or VL with 6% hydroxyethyl starch 130/0.4 was administered prior to elective surgery in patients of good cardiopulmonary health (n =9 in each group). We measured concentrations of ANP in plasma and of three main constituent parts of the glycocalyx (hyaluronan, heparan sulfate and syndecan 1) in serum before and after ANH or VL. Heparan sulfate and syndecan 1 levels in urine were also determined.ResultsIn contrast to ANH, VL (20 ml/kg) induced a significant release of ANP (approximately +100%, P ConclusionThese data suggest that hypervolemia increases the release of ANP and causes enhanced shedding of the endothelial glycocalyx. This perturbation must be expected to impair the vascular barrier, implying that VL may not be as safe as generally assumed and that it should be critically evaluated.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 25497357 · DOI · PMC4201669
Structure and function of the Nppa-Nppb cluster locus during heart development and disease [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Atrial natriuretic factor and brain natriuretic peptide are two important biomarkers in clinical cardiology.
- Closing excerpt
- In this review, we will provide recent insights into the dynamic and complex regulation of Nppa and Nppb during heart development and hypertrophy, and the association of this gene cluster with the cardiomyocyte-intrinsic program of heart regeneration.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (146 words)
Atrial natriuretic factor and brain natriuretic peptide are two important biomarkers in clinical cardiology. These two natriuretic peptide hormones are encoded by the paralogous genes Nppa and Nppb, which are evolutionary conserved. Both genes are predominantly expressed by the heart muscle during the embryonic and fetal stages, and in particular Nppa expression is strongly reduced in the ventricles after birth. Upon cardiac stress, Nppa and Nppb are strongly upregulated in the ventricular myocardium. Much is known about the molecular and physiological ques inducing Nppa and Nppb expression; however, the transcriptional regulatory mechanisms of the Nppa-Nppb cluster in vivo has proven to be quite complex and is not well understood. In this review, we will provide recent insights into the dynamic and complex regulation of Nppa and Nppb during heart development and hypertrophy, and the association of this gene cluster with the cardiomyocyte-intrinsic program of heart regeneration.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 29302701 · DOI · PMC5852170
Role of Cardiac Natriuretic Peptides in Heart Structure and Function [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Cardiac natriuretic peptides (NPs), atrial NP (ANP) and B-type NP (BNP) are true hormones produced and released by cardiomyocytes, exerting several systemic effects.
- Closing excerpt
- This narrative review is focused on the direct activities of this molecule family on the heart, reporting both experimental and human studies that are clinically relevant for physicians.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (148 words)
Cardiac natriuretic peptides (NPs), atrial NP (ANP) and B-type NP (BNP) are true hormones produced and released by cardiomyocytes, exerting several systemic effects. Together with C-type NP (CNP), mainly expressed by endothelial cells, they also exert several paracrine and autocrine activities on the heart itself, contributing to cardiovascular (CV) health. In addition to their natriuretic, vasorelaxant, metabolic and antiproliferative systemic properties, NPs prevent cardiac hypertrophy, fibrosis, arrhythmias and cardiomyopathies, counteracting the development and progression of heart failure (HF). Moreover, recent studies revealed that a protein structurally similar to NPs mainly produced by skeletal muscles and osteoblasts called musclin/osteocrin is able to interact with the NPs clearance receptor, attenuating cardiac dysfunction and myocardial fibrosis and promoting heart protection during pathological overload. This narrative review is focused on the direct activities of this molecule family on the heart, reporting both experimental and human studies that are clinically relevant for physicians.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 36430893 · DOI · PMC9697447
Single intramuscular injection of self-amplifying RNA of Nppa to treat myocardial infarction [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Self-amplifying RNA (saRNA) enables sustained protein expression from a single administration.
- Closing excerpt
- Together, these results demonstrate that one-shot saNppa-LNP therapy offers durable cardioprotection, supporting the broader potential of saRNA-LNP-based approaches for cardiac therapy.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (131 words)
Self-amplifying RNA (saRNA) enables sustained protein expression from a single administration. In this study, we developed an intramuscular saRNA-lipid nanoparticle (saNppa-LNP) therapy encoding natriuretic peptide type A (Nppa) for cardioprotection. A single injection induced sustained pro-atrial natriuretic peptide (pro-ANP) secretion for 4 weeks; pro-ANP was subsequently cleaved by the cardiac protease corin into active ANP, producing robust cardioprotection in mouse and swine myocardial infarction models. At equivalent doses, saNppa achieved greater efficacy than conventional mRNA. Single-nucleus transcriptomics identified natriuretic peptide receptor 1-positive (Npr1+) endothelial and epicardial cells as primary effectors, with saNppa-LNPs reshaping their paracrine profile to promote cardiomyocyte regeneration and suppress fibrosis. Longitudinal biosafety assessments revealed no systemic toxicity. Together, these results demonstrate that one-shot saNppa-LNP therapy offers durable cardioprotection, supporting the broader potential of saRNA-LNP-based approaches for cardiac therapy.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41785353 · DOI · PMC13124201
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Natriuretic peptides [5]
- Research article Natriuretic peptides [6]
- Research article Cardiac natriuretic peptides [7]
- Research article Atrial natriuretic peptide: synthesis, release, and metabolism [8]
- Research article The diagnostic accuracy of the natriuretic peptides in heart failure: systematic review and diagnostic meta-analysis in the acute care setting [9]
- Research article Receptors of atrial natriuretic factor [10]
References
- Chappell D, Bruegger D, Potzel J, Jacob M, Brettner F, Vogeser M, et al.. Hypervolemia increases release of atrial natriuretic peptide and shedding of the endothelial glycocalyx. . 2014. PMID 25497357 · DOI · PMC4201669
- Man J, Barnett P, Christoffels VM. Structure and function of the Nppa-Nppb cluster locus during heart development and disease. . 2018. PMID 29302701 · DOI · PMC5852170
- Sarzani R, Allevi M, Di Pentima C, Schiavi P, Spannella F, Giulietti F. Role of Cardiac Natriuretic Peptides in Heart Structure and Function. . 2022. PMID 36430893 · DOI · PMC9697447
- Zhang K, Tao H, Zhu D, Yue Z, Hu S, Wu Y, et al.. Single intramuscular injection of self-amplifying RNA of Nppa to treat myocardial infarction. . 2026. PMID 41785353 · DOI · PMC13124201
- Levin ER, Gardner DG, Samson WK. Natriuretic peptides. N Engl J Med. 1998. PMID 9682046 · DOI
- Daniels LB, Maisel AS. Natriuretic peptides. J Am Coll Cardiol. 2007. PMID 18154959 · DOI
- Goetze JP, Bruneau BG, Ramos HR, Ogawa T, de Bold MK, de Bold AJ. Cardiac natriuretic peptides. Nat Rev Cardiol. 2020. PMID 32444692 · DOI
- Ruskoaho H. Atrial natriuretic peptide: synthesis, release, and metabolism. Pharmacol Rev. 1992. PMID 1480667 · DOI
- Roberts E, Ludman AJ, Dworzynski K, Al-Mohammad A, Cowie MR, McMurray JJ, et al.. The diagnostic accuracy of the natriuretic peptides in heart failure: systematic review and diagnostic meta-analysis in the acute care setting. BMJ. 2015. PMID 25740799 · DOI · PMC4353288
- Maack T. Receptors of atrial natriuretic factor. Annu Rev Physiol. 1992. PMID 1532887 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.