International union of pharmacology. XXIII. The angiotensin II receptors.
By M. Gasparo, K. Catt, T. Inagami, J. Wright, T. Unger. Pharmacological Reviews, 2000
2,189 citations recorded by the source corpus.
The cardiovascular and other actions of angiotensin II (Ang II) are mediated by AT(1) and AT(2) receptors, which are seven transmembrane glycoproteins with 30% sequence similarity. Most species express a single autosomal AT(1) gene, but two related AT(1A) and AT(1B) receptor genes are expressed in rodents. AT(1) receptors are predominantly coupled to G(q/11), and signal through phospholipases A, C, D, inositol phosphates, calcium channels, and a variety of serine/threonine and tyrosine kinases. Many AT(1)-induced growth responses are mediated by transactivation of growth factor receptors. The receptor binding sites for agonist and nonpeptide antagonist ligands have been defined. The latter compounds are as effective as angiotensin converting enzyme inhibitors in cardiovascular diseases but are better tolerated. The AT(2) receptor is expressed at high density during fetal development. It is much less abundant in adult tissues and is up-regulated in pathological conditions. Its signaling pathways include serine and tyrosine phosphatases, phospholipase A(2), nitric oxide, and cyclic guanosine monophosphate. The AT(2) receptor counteracts several of the growth responses initiated by the AT(1) and growth factor receptors. The AT(4) receptor specifically binds Ang IV (Ang 3-8), and is located in brain and kidney. Its signaling mechanisms are unknown, but it influences local blood flow and is associated with cognitive processes and sensory and motor functions. Although AT(1) receptors mediate most of the known actions of Ang II, the AT(2) receptor contributes to the regulation of blood pressure and renal function. The development of specific nonpeptide receptor antagonists has led to major advances in the physiology, pharmacology, and therapy of the renin-angiotensin system.
Subfields: Cardiology and Cardiovascular Medicine, Endocrinology, Diabetes and Metabolism, Pharmacology
View Paper: https://www.semanticscholar.org/paper/612e6c6c8e0af836b17610bbe6f59d006f32194e
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In Cardiology and Cardiovascular Medicine
In Endocrinology, Diabetes and Metabolism
Citations in the corpus
- ADAMs as mediators of EGF receptor transactivation by G protein-coupled receptors. (2006, background): “A cardiovascular hormone, ANG II, signals mainly through the angiotensin type I (AT1) receptor (17, 35, 95, 102, 113).”
- Molecular distinction between physiological and pathological cardiac hypertrophy: experimental findings and therapeutic strategies. (2010, background): “Ang II is the principal vasoactive substance of the renin–angiotensin system with a variety of pathophysiological actions in the cardiovascular system via systemic and local effects including vasoconstriction, aldosterone release, and cell growth (Zimmerman & Dunham, 1997; de Gasparo et al., 2000).”
- Structural Basis for Ligand Recognition and Functional Selectivity at Angiotensin Receptor*♦ (2015, background): “Overstimulation of AT1R leads to diseases such as hypertension, cardiovascular hypertrophy, and fibrosis, whereas blocking the activity of AT1R lowers blood pressure (3, 4).”
- Angiotensin II revisited: new roles in inflammation, immunology and aging (2010, background): “Finally, the AT1 andAT2 receptors are also binding site for Ang III, while the AT4 receptor is specific for Ang IV and is expressed in brain, kidney, heart and vessels (de Gasparo et al, 2000).”
- Regulation of coronary blood flow during exercise. (2008, background): “However, even when systemic hemodynamic effects are avoided by intracoronary administration of the AT1 antagonist (457, 475), myocardial oxygen demands can be reduced as a result of a decrease in contractility both directly, through blockade of AT1 receptors on the cardiomyocytes (125), and indirect”