A
atrial natriuretic peptide receptor is a
receptor for
atrial natriuretic peptide.
Mechanism
NPRA and NPRB are linked to
guanylyl cyclases, while NPRAC 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...
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