D uring the past two decades we have witnessed our view of the renin-angiotensin system expand in a major way. Although originally perceived as a classical humoral system in which biologically active molecules are secreted from a dedicated gland to reach their target tissues via the bloodstream, a number of observations have indicated that local renin-angiotensin systems, complete with respect to all the components of the enzymatic pathway, may reside within individual organs or tissues. The existence of these so-called tissue renin-angiotensin systems, still conjectural at the beginning of the 1980s, has become muchmore firmly established during the past decade. 1'2We owe this, in large part, to the advent of molecular biological methods that, for the first time, allowed unequivocal confirmation of local synthesis of the elements comprising the renin-angiotensin system's catalytic cascade in a number of extrarenal tissues. In parallel, observations based primarily on the use of drugs interfering with the renin-angiotensin system have stimulated interest in the pathophysiological importance of local renin-angiotensin systems. This article will examine the evidence for, and the potential physiological and pathophysiological importance of, such a local renin-angiotensin system in the heart. The remarkable effectiveness of converting enzyme inhibition in heart failure, which has brought major progress in the therapy of this common and lethal affliction, and the mounting evidence for additional cardioprotective effects of these drugs have sparkedparticular interest in a cardiac tissue renin-angiotensin system and its role in normal and diseased states. This year marks the fiftieth anniversary of the first demonstration of a direct interaction between the renin-angiotensin system and the heart3; since then,