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Angiotensin-Converting Enzyme Inhibitors in Acute Coronary Syndromes

  • Antonio Rosado
  • Gervasio A. Lamas
Part of the Contemporary Cardiology book series (CONCARD)

Abstract

A century ago, Tigerstedt and Bergman (1) infused extracts of rabbit kidney into experimental animals and noted a hypertensive response. The chemical effector in the extracts would later be named renin. Years later, in another landmark study, Goldblatt et al. (2) produced systemic hypertension in dogs by clipping their renal artery, further supporting the hypothesis that the kidneys played a central role in blood pressure regulation. It was not, however, until the 1950s that the bloodborne complement of enzymes and substrates comprising the renin-angiotensin system would be elucidated. We now understand that renal juxtaglomerular cells secrete renin in response to intravascular volume depletion, decreased serum sodium concentration, and adrenergic stimulation. In the bloodstream, renin proteolytically cleaves the prohormone angiotensinogen, produced and secreted by the liver, into the decapeptide angiotensin I. Angiotensin I, in turn, is cleaved into the octapeptide angiotensin II by angiotensin-converting enzyme (ACE), a ubiquitous enzyme present on the surface of endothelial cells. The many important effects of the renin-angiotensin system discussed in this chapter may be attributed to the action of angiotensin II on its receptors in multiple organs (Fig. 1).

Keywords

Myocardial Infarction Acute Coronary Syndrome Left Ventricular Dysfunction Anterior Myocardial Infarction Infarct Expansion 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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© Springer Science+Business Media New York 1999

Authors and Affiliations

  • Antonio Rosado
  • Gervasio A. Lamas

There are no affiliations available

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