Angiotensin AT2 receptor: the younger sibling attracts attention

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Abstract
See article by Caballero et al. [6] (pages 86–95) in this issue . Electrical remodeling is a crucial aspect of the general process of cardiac remodeling associated with left ventricular hypertrophy and heart failure [1], and it is thought to contribute to an increased risk of ventricular fibrillation and sudden cardiac death. Angiotensin II has long been recognized as a major factor in cardiac remodeling in a variety of cardiovascular and non-cardiovascular diseases—from hypertension to diabetes [2]. Two receptor subtypes for angiotensin II have been identified in the heart, AT1 and AT2, which apparently share two features: the endogenous ligand and the gross molecular structure, belonging both to the seven transmembrane-domain receptor family [3]. Because of its well-documented action on myocyte hypertrophy, collagen deposition, aldosterone production, and many other functions, the AT1 receptor has long monopolized the attention of researchers [4]. Experimental observations have provided the rationale for development and clinical use of angiotensin receptor blockers (ARB), with the aim of offering a better protection than angiotensin-converting enzyme inhibitors (ACE-I) against angiotensin II by directly blocking AT1. Due to the activity of peptidases other than ACE (e.g., chymase) that convert angiotensin I to angiotensin II, ACE-I block less than 15% of the total production of angiotensin II in the heart. The number of patients receiving ACE-I is … *Corresponding author. Tel.: +39-554271264; fax: +39-554271285. Email address: alessandro.mugelli{at}unifi.it

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