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Class of antihypertensives that bind to and inhibit the angiotensin II receptor type 1 and thereby block the arteriolar contraction and sodium retention effects of renin–angiotensin system. Azilsartan medoxomil; Candesartan; Eprosartan; Fimasartan; Irbesartan; Losartan; Olmesartan; Telmisartan; Valsartan
Antihypertensive agents comprise multiple classes of compounds that are intended to manage hypertension (high blood pressure). Antihypertensive therapy aims to maintain a blood pressure goal of <140/90 mmHg in all patients, as well as to prevent the progression or recurrence of cardiovascular diseases (CVD) in hypertensive patients with established CVD. [2]
Angiotensin II receptor type 1 (AT1) is a G q/11-coupled G protein-coupled receptor (GPCR) and the best characterized angiotensin receptor. It is encoded in humans by the AGTR1 gene. AT1 has vasopressor effects and regulates aldosterone secretion. It is an important effector controlling blood pressure and volume in the cardiovascular system.
Class II agents are conventional beta blockers. They act by blocking the effects of catecholamines at the β 1-adrenergic receptors, thereby decreasing sympathetic activity on the heart, which reduces intracellular cAMP levels and hence reduces Ca 2+ influx. These agents are particularly useful in the treatment of supraventricular tachycardias.
AT 2 receptors are more plentiful in the fetus and neonate. The AT 2 receptor remains enigmatic and controversial – is probably involved in vascular growth. Effects mediated by the AT 2 receptor are suggested to include inhibition of cell growth, fetal tissue development, modulation of extracellular matrix, neuronal regeneration, apoptosis, cellular differentiation, and maybe vasodilation ...
Alpha 2 blockers. Alpha 2 blockers inhibit the activation of adenylyl cyclase via Gi protein by antagonising alpha 2 receptors, which curbs the synthesis of cyclic AMP (cAMP). [1] This subsequently reduces the concentration of calcium and the release of neurotransmitters, resulting in smooth muscle dilation. [1] Beta 1 blockers
This also turned out to be a misnomer: arrestin-1 expresses at comparable very high levels in both rod and cone photoreceptor cells. Arrestin-2 was the first non-visual arrestin cloned. It was first named β-arrestin simply because of the two GPCRs available in purified form at the time, rhodopsin and β 2 -adrenergic receptor , it showed ...
The alpha-2 blocker acts on alpha-2 receptors. The alpha-2 receptor is a G-protein coupled receptor as well, which exert its action by Gi function, leading to an inhibition of adenylyl cyclase and thus reducing synthesis of cAMP. [3] It lowers the amount of calcium inside the cell. [3]