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Anti-adrenergic effects of angiotensin converting enzyme inhibitors
1Division of Cardiology, University of Colorado Health Sciences Center, Denver, USA.
Abstract:
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.
Insights
In heart failure, the renin-angiotensin and adrenergic systems amplify each other, causing damage. Inhibiting one system, like with angiotensin converting enzyme inhibitors, can reduce the other
Area of Science:
- Cardiovascular Physiology
- Cardiac Pathophysiology
- Neuroendocrinology
Background:
- The failing heart activates compensatory renin-angiotensin and adrenergic systems.
- These systems are cross-regulated, leading to co-amplification of detrimental cellular and chamber remodeling.
- Chronic activation results in myocyte dysfunction and ventricular dilatation.
Purpose of the Study:
- To investigate the cross-regulation between the renin-angiotensin and adrenergic systems in heart failure.
- To explore the therapeutic potential of inhibiting these systems.
Main Methods:
- Review of existing literature on cardiac compensatory mechanisms.
- Analysis of the interplay between renin-angiotensin and adrenergic signaling in ventricular myocardium.
- Examination of the effects of angiotensin converting enzyme inhibitors.
Main Results:
- Activation of one system (renin-angiotensin or adrenergic) induces the other in the failing heart.
- This co-amplification promotes myocyte hypertrophy, hyperplasia, and increased cardiac output.
- Chronic activation leads to adverse cardiac remodeling and myocyte dysfunction.
- Inhibition of one system attenuates the activity of the other, particularly in heart failure.
Conclusions:
- Angiotensin converting enzyme inhibitors demonstrate anti-adrenergic effects in heart failure.
- These anti-adrenergic properties contribute to the beneficial clinical outcomes of ACE inhibitors in heart failure and ischemic heart disease.
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