"Tissue ACE" Properties: Nothing to Sneeze At?

Lately I have heard that "tissue ACE" properties are important in endothelial remodelingand in the prevention of myocardial infarction and stroke. What is theclinical relevance of these properties--and which angiotensin-converting enzyme(ACE) inhibitor is indeed a tissue ACE inhibitor?
---- Marc Grobman, DO
Wilmington, Del
The circulating renin-angiotensin-aldosterone system is responsible forthe acute changes that prevent circulating volume loss--increased sympatheticdrive, vasoconstriction, augmentation of cardiac output, intensificationof thirst, and sodium and water retention. These changes arecaused by the action of angiotensin II on blood vessels, brain, adrenalglands, and kidneys. Angiotensin II stimulates components of the renin-angiotensin-aldosterone system within the tissues of these organs to promote vascularhypertrophy, left ventricular hypertrophy, and glomerular hypertrophy.The converting enzyme inhibitors that have greater potency in inhibitingtissue ACE include quinapril, trandolapril, benazepril, ramipril, and perindopril.One might hypothesize that these agents would be more effective at preventingtarget organ damage. However, ACE inhibitors with both greater andlesser ability to inhibit tissue ACE have been shown to reduce cardiovascularevents (including myocardial infarction, stroke, and congestive heart failure)and renal insufficiency.No outcome studies have directly compared the more potent tissue ACE inhibitorswith those that are less potent. Until such studies are performed, potencyin the inhibition of tissue ACE is not a reason to choose a particular agent. Irecommend that you base your selection on the patient's condition and whetherthe ACE inhibitor you are considering reduces morbidity and mortality in thatsetting.
---- L. Michael Prisant, MD
Professor of Medicine
Director of Hypertension & Clinical Pharmacology
Medical College of Georgia
Augusta