Abstract
Over the last three decades, great strides have been made in our understanding of the pathophysiology of congestive heart failure, particularly with regard to the central role of the renin—angiotensin system (RAS), which is activated early in the course of heart failure. These findings are highlighted by recent studies that demonstrate improved survival in patients with heart failure and left ventricular dysfunction treated with angiotensin-converting enzyme (ACE) inhibitors.1–3 However, questions remain about the specificity of these agents for blocking the RAS. Angiotensin II (ANG II), which is central to the activity of this important system, exerts numerous effects on a variety of vascular and nonvascular tissues due to the activation of specific ANG II receptors on the cell surface.4–6 The recent development of specific AT1 receptor antagonists (AT1A) and the ability to analyze receptor numbers allow investigation of the central role of AT1 receptors in modulating the effects of activation of the RAS in heart failure.
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Fitzpatrick, M.A., Rademaker, M., Espiner, E.A. (1994). Angiotensin II Receptor Antagonism in an Ovine Model of Heart Failure Comparison with ACE and Renin Inhibition. In: Saavedra, J.M., Timmermans, P.B.M.W.M. (eds) Angiotensin Receptors. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2464-9_15
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DOI: https://doi.org/10.1007/978-1-4615-2464-9_15
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