Atrial natriuretic peptide receptor
Encyclopedia
A atrial natriuretic peptide receptor is a receptor for atrial natriuretic peptide
.
, 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 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.
Atrial natriuretic peptide
Atrial natriuretic peptide , atrial natriuretic factor , atrial natriuretic hormone , or atriopeptin, is a powerful vasodilator, and a protein hormone secreted by heart muscle cells. It is involved in the homeostatic control of body water, sodium, potassium and fat...
.
Mechanism
NPRA and NPRB are linked to guanylyl cyclasesGuanylate cyclase
-Reaction:Guanylate cyclase catalyzes the reaction of guanosine triphosphate to 3',5'-cyclic guanosine monophosphate and pyrophosphate:-Types:...
, while NPRAC is G-protein
G protein-coupled receptor
G protein-coupled receptors , also known as seven-transmembrane domain receptors, 7TM receptors, heptahelical receptors, serpentine receptor, and G protein-linked receptors , comprise a large protein family of transmembrane receptors that sense molecules outside the cell and activate inside signal...
-linked and is a "clearance receptor" that acts to internalise and destroy the ligand.
ANP activation of the ANP catalytic receptor
Catalytic receptor
A Catalytic receptor is an integral membrane protein possessing both enzymatic catalytic and receptor functions.The following is a list of the five major families of catalytic receptors:...
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
Total peripheral resistance
Vasculature throughout the entire body can be thought of as two separate circuits - one is the systemic circulation, while the other is the pulmonary circulation. Total peripheral resistance is the sum of the resistance of all peripheral vasculature in the systemic circulation...
, which will in turn decrease venous return
Venous return
Venous return is the rate of blood flow back to the heart. It normally limits cardiac output.Superimposition of the cardiac function curve and venous return curve is used in one hemodynamic model.-Physiology:...
to the heart. The decrease in venous return to the heart will reduce the preload
Preload
In cardiac physiology, preload is the end volumetric pressure that stretches the right or left ventricle of the heart to its greatest geometric dimensions under variable physiologic demand...
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.