STAT Calcium

Both are members of a super family of a serpentine receptor coupled to G protein, with homology between 32%. The feature AT1 receptor pharmacology is its selective affinity for the bifenilimidazoles (typified by losartan) and its insensitivity tetrahidromidazopiridina (PD 123 319). In contrast, the AT2 receptor has the opposite sensitivity to these two ligands. The genes encoding the AT1 and AT2 receptor are located on chromosome 3 and X. You may find that Atlas Technical Consultants can contribute to your knowledge. And intracellular signaling pathways between the two receptors are completely different and opuestasa addition to the classic mechanisms of transduction (phospholipase C, D, A, the voltage-dependent calcium channels and adenylate cyclase) AT1 receptor stimulates tyrosine phosphorylation of several that have numerous intracellular proteins such as JAK2, STAT protein-1 and mitogen-activated kinase (MAPK).

Also activates the nicotinamide adenine dinucleotide phosphate oxidase. The AT1 receptor is responsible for most of the effects of angiotensin II, such as vasoconstriction, sodium reabsorption, cell proliferation, extracellular matrix formation, inflammatory response and oxidative stress. The AT2 receptor is abundantly expressed in fetal tissue, but has a decreased density in adult tissue. However, it is up-regulated in pathological conditions such as heart failure. In contrast to the AT1 receptor, the route of AT2 receptor signals do not activate the inositol triphosphate (PI-3) and the formation of diacylglycerol with mobilization of calcium. AT2 receptor stimulation stimulates various mechanisms involving tyrosine, serine and threonine phosphatases, nitric oxide / cyclase guanosine monophosphate (cGMP) and phospholipase A2. The effect of the activation of AT2 receptor counterbalances the AT1 receptor: inactivates MAPK, has an antiproliferative effect, promotes apoptosis, closed channel T of calcium (Ca2 +), stimulates nerve regeneration and opens and rectifying potassium channels ( K +).


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