Atrial natriuretic peptide

  • OMIM: 108780
  • MGI: 97367

Atrial natriuretic peptide (ANP, also known as atrial natriuretic factor (ANF ), older names are atriopeptin, natriuretic peptide type A, Cardionatrine, CDD, cardiodilatin or atrial natriuretic factor ), is a peptide hormone that for the most part of the muscle cells ( myocytes ) of the atria (atrium ) will be paid due to strain stimuli. It causes an increase in urinary excretion. Linked to this is a sodium ion ausschwemmende ( natriuretic ) effects.

The amount of hormone level was partially considered as an indication of the severity of heart failure, however, has to reach no diagnostic value. In clinical practice, the related BNP has prevailed.

Adolfo J. de Bold and his team discovered ANP 1981 in Canada.

Biosynthesis

The ANP gene has three exons and two introns, it encodes a 151 amino acid pre-pro ANP large, from which, by splitting off an N-terminal signal peptide (25 amino acids) is pro-ANP. Corin, a membrane-bound serine protease, cleaves the C -terminus of ANP from (28 amino acids). The beginning and the end are closed by a disulfide bond to form a ring. Except in the heart is the synthesis to a lesser extent also taking place in the brain, adrenal gland and kidney. The Urodilatin formed in collecting duct cells from pro- ANP contains 32 amino acids and is biologically stable than ANP. Another peptide, which is cleaved from Pro -ANP is cardiodilatin (CDP). Two related natriuretic peptides, which are encoded by different genes, are BNP and CNP.

Physiology and Biochemistry

ANP is secreted increased at elevated pressure and stretching of the atrial wall. It is (or more precisely to the lowering of blood pressure ) involved in blood pressure regulation. It acts both in the kidney and in the smooth muscle of the arterioles.

The ANP is a vasodilator neurotransmitter. It caused by activation ( binding of ANP / BNP as a ligand in the A receptor, CNP at B receptor and homodimerization ) of membrane-bound guanylyl an increase in intracellular cGMP concentration. cGMP activates cGMP-dependent protein kinase ( PRKG1 ) which is activated by phosphorylation of ATP-dependent calcium pumps in the cell membrane. Calcium ions are transported out of the cell increases. This leads to smooth muscle relaxation. Further binds ANP ( BNP and CNP) to another transmembrane receptor (C- receptor ), whose activation does not lead to a cGMP increase and for a clearance function, it is assumed that binds so excess ANP and an intracellular degradation feeds.

ANP is also effective in the kidney: It reduces the sodium recovery and thereby leading to increased excretion of sodium and chloride. Since sodium chloride is osmotically active, water follows. By vasodilation in the glomerular blood vessels, the filtration rate is enhanced. This leads to an increased urinary excretion and reduced plasma volume. A reduction in plasma volume also results in decreased blood pressure. In the arterioles ANP leads indirectly, on the reduction of renin concentration, vasodilation. In the hypothalamus, the feeling of thirst is inhibited by ANP. In the pituitary ADH secretion decreased.

A further effect is the inhibition of the renin- angiotensin-aldosterone system by the release of renin and aldosterone both is reduced.

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Human Genome Organisation Mouse Genome Informatics Euteleostomi Entrez Ensembl UniProt National Center for Biotechnology Information Brain Natriuretic Peptide Cyclic guanosine monophosphate Adenosine triphosphate Renin–angiotensin system Digital Object Identifier
4436
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