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Review
. 2015 Sep 10;569(1):1-6.
doi: 10.1016/j.gene.2015.06.029. Epub 2015 Jun 12.

Atrial natriuretic peptide in cardiovascular biology and disease (NPPA)

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Review

Atrial natriuretic peptide in cardiovascular biology and disease (NPPA)

Wei Song et al. Gene. .

Abstract

Atrial natriuretic peptide (ANP) is a cardiac hormone that regulates salt-water balance and blood pressure by promoting renal sodium and water excretion and stimulating vasodilation. ANP also has an anti-hypertrophic function in the heart, which is independent of its systemic blood pressure-lowering effect. In mice, ANP deficiency causes salt-sensitive hypertension and cardiac hypertrophy. Recent studies have shown that ANP plays an important role in regulating vascular remodeling and energy metabolism. Variants in the human NPPA gene, encoding the ANP precursor, are associated with hypertension, stroke, coronary artery disease, heart failure (HF) and obesity. ANP and related peptides are used as biomarkers for heart disease. Recombinant proteins and small molecules that enhance the ANP pathway have been developed to treat patients with HF. In this review, we discuss the role of ANP in cardiovascular biology and disease.

Keywords: ANP; Corin; Heart failure; Hypertension; Natriuretic peptides; Sodium homeostasis.

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Figures

Fig. 1
Fig. 1
ANP synthesis and processing. ANP is synthesized as prepro-ANP. The signal peptide is removed by signal peptidase. Pro-ANP is converted to active ANP by corin. A disulfide bond connects two Cys residues, forming a ring structure in ANP. Neutral endopeptidase (NEP) inactivates ANP. In the kidney, alternative processing by an unknown enzyme generates urodilatin.
Fig. 2
Fig. 2
Variants and a frameshift mutation in NPPA. The human NPPA gene consists of three exons and two introns. NPPA variants in the 5’ promoter region, exons 1 and 3, and the 3’ untranslated region are indicated. A frameshift mutation abolishes the stop codon, creating a mutant ANP with 12 extra amino acids at the C-terminus (ANP+12aa).

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