Atrial Natriuretic Peptides (ANP/ANF) and Related Peptides

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Introduction

Atrial natriuretic peptide (ANP), also known as atrial natriuretic factor (ANF), plays an essential role in the regulation of blood pressure through the balance of water and salt metabolism. Generally, the common ANP is ANP_99-126, which contains 28 amino acids. The synthesis and secretion of ANP are mainly in the atria. The level of ANP in the central ventricle of adults is very low, but ANP has a marked increase in central ventricular tissue in the fetus and newborn. And ANP has also been detected in the central nervous system, lung, adrenal gland, kidney, and vascular tissue. There are three specific receptors for ANP: NPRA, NPRB, NPRC.

Mechanism of action

ANP is responsible for natriuresis, diuresis, and the regulation of water-salt balance, which is achieved by directly or indirectly altering renal hemodynamics. ANP binds to functional receptors in the medullary collecting duct (MCD) epithelial cells to produce cyclic guanosine monophosphate (cGMP), which controls the amiloride-sensitive sodium channel on the luminal side membrane through the action of cGMP-dependent protein kinase, thereby inhibiting the reabsorption of sodium ions. At the same time, cGMP can inhibit the reabsorption of water by ANP in the collecting tube. In addition to MCD, high concentration of ANP can contract the small arterioles, dilate the afferent glomerular arteriole, and increase the glomerulus filtration rate and filtration fraction, which enhances the sodium excretion of the kidney.

Application of Atrial Natriuretic Peptides (ANP/ANF) and Related Peptides

Hypertension will lead to increased pressure in the atria and ventricle, and may increase in blood volume due to renal drainage and sodium dysfunction, which stimulate the synthesis and release of ANP. ANP is able to lower blood pressure by diuresis, dilating of blood vessels and reducing peripheral resistance. It is found that the level of ANP are significantly increased in cardiovascular diseases such as hypertension, indicating that the synthesis and secretion of ANP may be a compensatory and protective response in a pathological state.

References

1. Baxter J D, Lewicki J A, Gardner D G. Atrial Natriuretic Peptide[J]. Nature Biotechnology, 1988, 37(6):529-546.
2. Rydén M, B?ckdahl J, Petrus P, et al. Impaired atrial natriuretic peptide-mediated lipolysis in obesity[J]. Int J Obes, 2016, 40(4):714-720.