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|Title:||Role of angiotensin II receptor antagonists in the treatment of hypertension||Authors:||Zhu, Y.Z.
|Issue Date:||1999||Citation:||Zhu, Y.Z., Lee, H.S. (1999). Role of angiotensin II receptor antagonists in the treatment of hypertension. Cor Europaeum - European Journal of Cardiac Interventions 7 (4) : 161-166. ScholarBank@NUS Repository.||Abstract:||Angiotensin II (ANG II), the most important effector peptide of the renin-angiotensin system (RAS), has been implicated in the pathology of hypertension, in cardiovascular diseases such as cardiac left ventricular hypertrophy (LVH) or neointima formation, and in structural alterations of the heart such as post-infarct remodeling. The recent development of specific, highly selective, non-peptide ANG II receptor antagonists/ligands was the basis for the identification of the ANG II receptor subtypes, designated AT1 and AT2. The characterization of two subtypes of the angiotensin receptor has offered new tools for advancing our knowledge of the mechanisms of hypertension and related diseases. The AT1 receptor is well characterized, but the role of AT2 receptor is still unclear. Most of the effects of ANG II, including the hypertensive ones, such as vasoconstriction and hypertrophy of vascular and cardiac smooth muscle cells, have been linked to AT1 receptor stimulation. The AT1 receptor is coupled to G-proteins and stimulates classical intracellular second messenger system such as inhibition of adenylate cyclase or activation of phospholipase C. The function of the AT2 receptor as well as its signal transduction mechanisms are still far from being understood. Due to its wide distribution in foetal tissues and its transient reappearance in the adult organism under pathological conditions, e.g. myocardial infarction, the AT2 receptor has been associated with cell differentiation and regeneration.||Source Title:||Cor Europaeum - European Journal of Cardiac Interventions||URI:||http://scholarbank.nus.edu.sg/handle/10635/133962||ISSN:||09398147|
|Appears in Collections:||Staff Publications|
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