Atrial natriuretic peptide receptor

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

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

NPR1
NPR1 or NPRA is encoded by the gene.

NPR2
NPR2 or NPRB is encoded by the gene.

NPR3
NPR3 or NPRC is encoded by the gene.

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.