ANP
The atrial pressure sensor — the first discovered natriuretic peptide, maintaining blood pressure and fluid balance through renal sodium excretion and vasodilation.
A 28-amino-acid cyclic peptide hormone released from atrial granules during atrial distension, activating NPR-A to produce natriuresis, vasodilation, and RAAS suppression.
Mechanism of action
Binds NPR-A (natriuretic peptide receptor A), a transmembrane guanylyl cyclase, increasing intracellular cGMP in kidney, vasculature, and adrenal glands. Effects: afferent arteriolar dilation + efferent constriction (increases GFR), suppresses aldosterone secretion, relaxes vascular smooth muscle, inhibits cardiac fibrosis.
Primary uses
- Blood pressure and volume regulation (physiological)
- Acute heart failure (carperitide, Japan)
- Cardiac physiology research
- Renal hemodynamics studies
Typical dosing
Endogenous hormone. Carperitide (Japan) dosed at 0.025–0.05 mcg/kg/min IV infusion.
Regulatory status
Native ANP not FDA-approved. Carperitide (recombinant ANP, marketed as Hanp) is approved in Japan for acute heart failure. Anaritide (synthetic ANP analog) was studied in US trials but not approved.
References
- [pubmed] de Bold AJ, et al. "A rapid and potent natriuretic response to intravenous injection of atrial myocardial extract in rats." Life Sci, 1981;28:89-94.
- [review] Potter LR, et al. "Natriuretic peptides, their receptors, and cyclic guanosine monophosphate-dependent signaling functions." Endocr Rev, 2006;27:47-72.
Related peptides
This entry is for educational purposes only and does not constitute medical advice. Dosing information reflects published regulatory or research data and is not a recommendation. Many compounds described here are not approved for human use in the United States. Consult a licensed medical professional before considering any peptide therapy.