Anti-adrenergic effects of angiotensin converting enzyme inhibitors

The renin-angiotensin and adrenergic nervous systems are cross-regulated compensatory mechanisms that are induced or activated in the failing heart. In ventricular myocardium, the activation of one of these systems leads to activation or induction of the other, resulting in co-amplification of cellular mechanisms that result in cardiac myocyte hypertrophy, hyperplasia of nonmyocytic tissue components, increased contractility and heart rate, and increased ventricular volume. Although these changes serve to stabilize stroke volume and cardiac output following an insult to the myocardium, the chronic and continual activation of these systems produces ventricular dilatation and deleterious remodelling at a chamber level and progressive myocyte dysfunction at a cellular level. Because these systems are cross-regulated inhibition of one of them attenuates the activity of the other. This appears to be especially true in the failing heart, where angiotensin converting enzyme inhibitors can produce substantial anti-adrenergic effects in individuals with high levels of adrenergic activation. The anti-adrenergic properties of angiotensin converting enzyme inhibitors may be at least partially responsible for the salutary effects of these agents in the clinical setting of heart failure or ischaemic heart disease.