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Published on: June 29, 2014
Prevention of structural changes in the heart in hypertension by angiotensin converting enzyme inhibition
1Department of Cardiovascular Studies, University of Leeds, Killingbeck Hospital, UK.
Insights
Angiotensin converting enzyme (ACE) inhibition prevents cardiac damage in hypertension models. ACE inhibitors like lisinopril reverse heart remodeling, including fibrosis and hypertrophy, improving heart function.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Hypertension Studies
Background:
- Hypertension leads to heart failure via myocyte loss and fibrosis.
- Cardioprotection and cardioreparation are key therapeutic goals.
- Understanding myocardial remodeling in hypertension is crucial.
Purpose of the Study:
- To determine if ACE inhibition influences myocardial remodeling in hypertension.
- To assess ACE inhibition for cardioprotective and cardioreparative effects.
Main Methods:
- Administered angiotensin II and induced renovascular hypertension in rats.
- Treated rats with genetic hypertension using high- and low-dose lisinopril.
- Evaluated cardiac myocyte necrosis, fibrosis, hypertrophy, and vascular changes.
Main Results:
- Angiotensin II infusion caused myocyte necrosis, preventable by ACE inhibition.
- Lisinopril normalized blood pressure, reversed hypertrophy and fibrosis in genetic hypertension.
- Low-dose lisinopril reversed fibrosis without significant blood pressure reduction.
Conclusions:
- ACE inhibition shows significant myocardial remodeling effects in experimental hypertension.
- ACE inhibitors offer potential for treating hypertensive heart disease.
- Targeting myocardial structure and function is a viable therapeutic strategy.
Background:
The long-term effects of hypertension on the heart culminate in congestive heart failure. The underlying causes are contractile impairment due to myocyte loss and reduced compliance due to myocardial fibrosis. Newer strategies in antihypertensive therapy must, therefore, focus on prevention of myocardial damage ('cardioprotection') or, if an abnormality has occurred, on reversal towards normal myocardial structure and function ('cardioreparation').
Objective:
To investigate the question of whether angiotensin converting enzyme (ACE) inhibition can influence myocardial remodelling in hypertension to produce cardioprotective and cardioreparative effects.
Methods And Results:
Infusion of pathophysiological levels of circulating angiotensin II in rats causes cardiac myocyte necrosis, followed by fibroblast proliferation. This necrosis is not secondary to adrenergic activation or raised blood pressure. Similarly, renovascular hypertension results in cardiac myocyte necrosis, which can be prevented by pretreatment with the ACE inhibitor captopril. In established genetic hypertension in rats, sustained treatment with high-dose lisinopril normalizes the blood pressure, reverses left ventricular hypertrophy, reverses excessive interstitial and perivascular fibrosis (and consequently the impaired compliance), and reverses excessive coronary artery medial thickening (thereby normalizing coronary vascular reserve). With a low dose of lisinopril that does not reduce blood pressure significantly, only the excessive fibrosis is reversed.
Conclusion:
ACE inhibition has demonstrated promising myocardial remodelling effects in experimental models of hypertensive heart disease.
Related Concept Videos
01:18Hypertension and Regulation of Blood Pressure
01:17Antihypertensive Drugs: Action of β1 Blockers
01:30Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors
01:30Antihypertensive Drugs: Angiotensin II Receptor Blockers
01:25Antihypertensive Drugs: Direct Renin Inhibitors
01:26Heart Failure Drugs: Inhibitors of Renin-Angiotensin System