Atrial Natriuretic Peptide
| Atrial Natriuretic Peptide | ||
|---|---|---|
|
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| 3D structure of an ANP variant. | ||
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Existing structural data: 1anp, 1yk0 |
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| Properties of human protein | ||
| Mass / length primary structure | 28 amino acids; 3.08 kDa | |
| Precursor | Prepronatriodilatin | |
| Identifier | ||
| Gene names | NPPA ; ANP; PND | |
| External IDs | ||
| Occurrence | ||
| Parent taxon | Euteleostomi | |
| Orthologue | ||
| human | mouse | |
| Entrez | 4878 | 230899 |
| Ensemble | ENSG00000175206 | ENSMUSG00000041616 |
| UniProt | P01160 | P05125 |
| Refseq (mRNA) | NM_006172 | NM_008725 |
| Refseq (protein) | NP_006163 | NP_032751 |
| Gene locus | Chr 1: 11.85 - 11.85 Mb | Chr 4: 148 - 148 Mb |
| PubMed search | 4878 |
230899
|
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 is mainly produced by muscle cells (myocytes ) of the atrium is released due to stretching stimuli. It causes an increase in urine output . This is coupled with a natriuretic effect that flushes out sodium ions.
The level of the hormone was partly taken as an indication of the severity of a heart failure , but has not reached any diagnostic value. In clinical practice, the related has BNP enforced
Adolfo J. de Bold and his team discovered ANP in Canada in 1981.
biosynthesis
The ANP gene has three exons and two introns ; it codes for a 151 amino acid prepro-ANP, which becomes pro-ANP by cleaving an N-terminal signal peptide (25 amino acids). Corin , a membrane-bound serine protease , cleaves ANP from the C-terminus (28 amino acids). The beginning and the end are closed to form a ring by a disulfide bridge. In addition to the heart, synthesis also takes place to a lesser extent in the brain , adrenal gland and kidney . The urodilatin formed in collecting tube cells from Pro-ANP contains 32 amino acids and is biologically more stable than ANP. Another peptide that is split off from Pro-ANP is cardiodilatin (CDP). Two related natriuretic peptides encoded by other genes are BNP and CNP .
Physiology and biochemistry
ANP is released to an increased extent with increased pressure and overstretching of the atrial wall. It is involved in blood pressure regulation (more precisely in lowering blood pressure). It works both in the kidneys and in the smooth muscles of the arterioles .
The ANP is a vasodilatory messenger substance. Activation (binding of ANP / BNP as a ligand to the A receptor, CNP to the B receptor and homodimerization) of membrane guanylyl cyclases causes an increase in the intracellular cGMP concentration. cGMP activates the cGMP-dependent protein kinase (PRKG1), which activates ATP- dependent calcium pumps in the cell membrane through phosphorylation . Calcium ions are increasingly transported out of the cell. This leads to the relaxation of the smooth muscles. Furthermore, ANP (BNP and CNP) binds to another transmembrane receptor (C-receptor), the activation of which does not lead to an increase in cGMP and for which a clearance function is assumed, which thus binds excess ANP and leads to intracellular degradation.
ANP also works in the kidneys: it reduces sodium recovery and thus leads to increased sodium and chloride excretion. Since sodium chloride is osmotically active, water follows. The rate of filtration is increased by vasodilation, also in the glomerular vessels. This leads to increased urine excretion and decreased plasma volume. A decrease in plasma volume also leads to decreased blood pressure. In the arterioles, ANP indirectly leads to vasodilation by lowering the renin concentration. In the hypothalamus, ANP suppresses the feeling of thirst. The release of ADH in the pituitary gland is reduced.
Another effect is the inhibition of the renin-angiotensin-aldosterone system by reducing the release of both renin and aldosterone .
Web links
Individual evidence
- ^ WJ Fairbrother, RS McDowell, BC Cunningham: Solution conformation of an atrial natriuretic peptide variant selective for the type A receptor . In: Biochemistry . 33, No. 30, August 1994, pp. 8897-8904. doi : 10.1021 / bi00196a006 . PMID 8043577 .
- ↑ Luchner et al .: Significance of the heart failure markers BNP and NT-proBNP for the clinic. In: Deutsches Ärzteblatt 2003; 100: Pages A 3314 - A 3321.
- ↑ T. Tokudome, I. Kishimoto, T. Horio et al. : Regulator of G-protein signaling subtype 4 mediates antihypertrophic effect of locally secreted natriuretic peptides in the heart . In: Circulation . 117, No. 18, May 2008, pp. 2329-2339. doi : 10.1161 / CIRCULATIONAHA.107.732990 . PMID 18443239 .