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ACE is a target of ACE inhibitor drugs, which decrease the rate of angiotensin II production. Angiotensin II increases blood pressure by stimulating the Gq protein in vascular smooth muscle cells (which in turn activates an IP3-dependent mechanism leading to a rise in intracellular calcium levels and ultimately causing contraction).
The angiotensin receptor is activated by the vasoconstricting peptide angiotensin II.The activated receptor in turn couples to G q/11 and G i/o and thus activates phospholipase C and increases the cytosolic Ca 2+ concentrations, which in turn triggers cellular responses such as stimulation of protein kinase C.
11609 Ensembl ENSG00000180772 ENSMUSG00000068122 UniProt P50052 P35374 RefSeq (mRNA) NM_000686 NM_001385624 NM_007429 RefSeq (protein) NP_000677 NP_031455 Location (UCSC) Chr X: 116.17 – 116.17 Mb Chr X: 21.35 – 21.36 Mb PubMed search Wikidata View/Edit Human View/Edit Mouse Angiotensin II receptor type 2, also known as the AT 2 receptor is a protein that in humans is encoded by the AGTR2 ...
However, when the blood circulates through the lungs a pulmonary capillary endothelial enzyme called angiotensin-converting enzyme (ACE) cleaves a further two amino acids from angiotensin I to form an octapeptide known as angiotensin II. Angiotensin II is a hormone which acts on the adrenal cortex, causing the release into the blood of the ...
Angiotensin II is the major bioactive product of the renin–angiotensin system, binding to receptors on intraglomerular mesangial cells, causing these cells to contract along with the blood vessels surrounding them; and to receptors on the zona glomerulosa cells, causing the release of aldosterone from the zona glomerulosa in the adrenal cortex.
The juxtaglomerular cells of the kidneys produce renin, which is a key regulator of the renin–angiotensin system, which is responsible for blood pressure regulation. [32] The production of erythropoietin by the kidneys is responsible for the differentiation of erythroid progenitor cells in the bone marrow into erythrocytes and is induced by ...
Inhibition of ACE with ACE inhibitors leads to decreased conversion of angiotensin I to angiotensin II (a vasoconstrictor) but also to an increase in bradykinin due to decreased degradation. This explains why some patients taking ACE inhibitors develop a dry cough, and some react with angioedema , a dangerous swelling of the head and neck region.
Contrastly, TXA 2 vascular tissue synthesis is stimulated by angiotensin II which promotes cyclooxygenase I's metabolism of arachidonic acid. An angiotensin II dependent pathway also induces hypertension and interacts with TXA 2 receptors.