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Atrial natriuretic peptide receptor

natriuretic peptide receptor A/ guanylate cyclase A (atrionatriuretic peptide receptor A)
Identifiers
Symbol NPR1
Alt. symbols ANPRA, NPRA
Entrez 4881
HUGO 7943
OMIM 108960
RefSeq NM_000906
UniProt P16066
Other data
Locus Chr. 1 q21-q22
natriuretic peptide receptor B/ guanylate cyclase B (atrionatriuretic peptide receptor B)
Identifiers
Symbol NPR2
Alt. symbols ANPRB, NPRB
Entrez 4882
HUGO 7944
OMIM 108961
RefSeq NM_003995
UniProt P20594
Other data
Locus Chr. 9 p21-p12
natriuretic peptide receptor C/ guanylate cyclase C (atrionatriuretic peptide receptor C)
Identifiers
Symbol NPR3
Alt. symbols ANPRC, NPRC
Entrez 4883
HUGO 7945
OMIM 108962
RefSeq NM_000908
UniProt P17342
Other data
Locus Chr. 5 p14-p1

An atrial natriuretic peptide receptor is a receptor for atrial natriuretic peptide.

NPRA and NPRB are linked to guanylyl cyclases, while NPRC is G-protein-linked and is a "clearance receptor" that acts to internalise and destroy the ligand.

ANP activation of the ANP catalytic receptor will stimulate its intracellular guanylyl cyclase activity to convert GTP to cGMP. cGMP will then stimulate cGMP-dependent protein kinase (PKG), which will then induce smooth muscle relaxation. This is particularly important in the vasculature, where vascular smooth muscle will bind ANP released as a result of increasing right atrial pressure and will cause the walls of the vasculature to relax. This relaxation will decrease total peripheral resistance, which will in turn decrease venous return to the heart. The decrease in venous return to the heart will reduce the preload and will result in the heart's having to do less work.

There is also a soluble guanylyl cyclase that cannot be stimulated by ANP. Instead, vascular endothelial cells will use L-arginine to make nitric oxide via nitric oxide synthase. The nitric oxide will then diffuse into the vascular smooth muscle and will activate the soluble guanylyl cyclase. The subsequent increase in cGMP will cause vasodilation with the same effects as described above. This is why nitroglycerine is given to a person having a heart attack. The nitroglycerine will be metabolized to nitric oxide, which will stimulate soluble guanylyl cyclase. This will result in a decrease in total peripheral resistance and a decrease in preload on the heart. As a result, work done by the heart will decrease and will allow the heart to contract less strongly. Weaker contractions will lead to more blood flow in the coronary arteries, which will help the ischemic cardiac myocytes.


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