Anatrial natriuretic peptide receptor is areceptor foratrial natriuretic peptide.[1]
NPRA and NPRB are linked toguanylyl cyclases, while NPRC isG-protein-linked and is a "clearance receptor" that acts to internalise and destroy the ligand.
ANP activation of the ANPcatalytic receptor will stimulate its intracellularguanylyl cyclase activity to convertGTP tocGMP. cGMP will then stimulatecGMP-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 decreasetotal peripheral resistance, which will in turn decreasevenous return to the heart. The decrease in venous return to the heart will reduce thepreload and will result in the heart's having to do less work.
There is also asoluble guanylyl cyclase thatcannot be stimulated by ANP. Instead, vascularendothelial 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 whynitroglycerine 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 thecoronary arteries, which will help the ischemic cardiac myocytes.
There are three distinctatrial natriuretic factor receptors identified so far in mammals: natriuretic peptide receptors 1, 2, and 3.
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