Atrial natriuretic peptide receptor

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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	NPRC, ANPRC
Entrez	4883
HUGO	7945
OMIM	108962
RefSeq	NM_000908
UniProt	P17342
Other data
Locus	Chr. 5 p14-p1

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

1 Types
2 Mechanism
3 External links

[edit] Types

There are three distinct atrial natriuretic factor receptors identified so far in mammals, natriuretic peptide receptors 1, 2 and 3.

[edit] NPR1

NPR1 or NPRA is encoded by the gene NPR1.

[edit] NPR2

NPR2 or NPRB is encoded by the gene NPR2.

[edit] NPR3

NPR3 or NPRC is encoded by the gene NPR3.

[edit] Mechanism

NPRA and NPRB are linked to guanylyl cyclases, while NPRAC is G-protein linked and furthermore is a "clearance receptor" which 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 them 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 having to do less work.

There is also a soluble guanylyl cyclase which CANNOT be stimulated by ANP. Instead, vascular endothelial cells with use L-citrullin to make nitrous oxide via nitrous oxide synthase. The nitrous 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 who is having a heart attack. The nitroglycerine will be metabolized to nitrous 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.