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(Circulation. 1997;95:1104-1107.)
© 1997 American Heart Association, Inc.

Articles

Downregulation of Angiotensin II Receptor Type 1 in Heart Failure

A Process of Adaptation or Deterioration?

Masahiko Kurabayashi, MD, PhD; Yoshio Yazaki, MD, PhD

From the Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo (Japan).

Correspondence to Yoshio Yazaki, MD, PhD, The Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113, Japan.

Key Words: Editorials • receptors, adrenergic, beta • angiotensin • heart failure

	Introduction

 
Among the major consequences of reduced cardiac performance is the neurohumoral response, mediated primarily by activation of the sympathetic-adrenergic system and the renin-angiotensin system (RAS). These responses may contribute to maintain homeostasis and are considered to be adaptive mechanisms to a fall in cardiac output for the short term. If sustained in heart failure, however, the cellular and molecular abnormality within the heart induced by these changes can cause detrimental effects on cardiac function and thus plays a critical part in determining the poor prognosis of this condition.¹ It is now apparent that cardiac hypertrophy, one of the most important responses of the failing heart, is a complex process that is both beneficial and detrimental. Although a growing number of molecular changes have been recognized in both compensatory hypertrophy and end-stage heart failure, it is poorly understood whether such changes contribute to or compensate for the deterioration of the heart or are simply associated with the failure and have nothing to do with the relevant processes. Thus, understanding the nature and mechanisms for the transition to heart failure after chronic overload has been a focus of considerable attention.

During the last several years we have witnessed a great advance in our understanding with respect to the pathophysiological role of the local RAS in the heart. Evidence presented to date indicates that the local RAS is selectively activated despite the normal circulating RAS in the overloaded heart associated with hemodynamic overload and myocardial infarction. Since angiotensin II exerts direct cardiac effects, . . . [Full Text of this Article]

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