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Cell biology and genetics of angiotensin in cardiovascular disease
1Falk Cardiovascular Research Center, Stanford University School of Medicine.
Insights
Angiotensin promotes vascular and cardiac growth, influencing cardiovascular disease. Angiotensin-converting enzyme (ACE) inhibitors show promise in preventing cardiac enlargement post-myocardial infarction.
Area of Science:
- Cardiovascular Physiology
- Molecular Biology
- Pharmacology
Background:
- Angiotensin, a vasoconstrictive peptide, is recognized for its role in vascular and cardiac growth.
- It directly impacts coronary artery disease and ventricular remodeling by activating growth factors.
- The presence of angiotensin-converting enzyme (ACE) and angiotensin II in vascular tissue implicates them in vascular lesion development.
Purpose of the Study:
- To explore the growth-promoting effects of angiotensin on vascular and cardiac tissues.
- To investigate the role of angiotensin and ACE in cardiovascular disease pathophysiology, including ventricular remodeling.
- To review the impact of ACE inhibitor therapy on cardiovascular outcomes.
Main Methods:
- Review of existing literature on angiotensin's effects on vascular and cardiac growth.
- Analysis of studies demonstrating the presence and role of ACE and angiotensin II in cardiovascular pathology.
- Examination of clinical trial data on ACE inhibitor therapy in post-myocardial infarction patients.
Main Results:
- Angiotensin activates autocrine/paracrine growth factors, modulating vascular growth.
- Cardiac tissue ACE is implicated in ventricular remodeling and heart failure.
- ACE inhibitor therapy has shown efficacy in reducing recurrent myocardial infarction and preventing cardiac enlargement post-MI.
Conclusions:
- Angiotensin plays a significant role in vascular and cardiac growth, contributing to cardiovascular disease.
- ACE inhibitors offer therapeutic benefits in managing post-myocardial infarction complications.
- Ongoing trials will further elucidate the long-term effects of ACE inhibitors on coronary events and atherosclerosis.
Abstract:
GROWTH-PROMOTING EFFECTS OF ANGIOTENSIN: Angiotensin, a vasoconstrictive peptide, is now known to be an agent of vascular and cardiac growth and may directly influence the pathophysiology of coronary artery disease and ventricular remodeling. Vascular growth occurs when angiotensin activates autocrine and paracrine growth factors, including fibroblast growth factor, transforming growth factor beta-1 and platelet-derived growth factor, and is modulated by endothelium-derived vasodilators and growth inhibitors. ANGIOTENSIN AND CARDIOVASCULAR DISEASE: The presence of angiotensin converting enzyme (ACE) and angiotensin II has been demonstrated in vascular tissue, and these local substances are causally involved in the development of vascular lesions. Similarly, angiotensin can stimulate cardiac myocyte growth and matrix modulation. Cardiac tissue ACE is implicated in ventricular remodeling in the course of progressive heart failure. A genetic variant of the ACE gene has been reported to be associated with increased risks of cardiovascular pathology. ACE INHIBITOR THERAPY: To date, studies of ACE inhibitor treatment in human patients have not demonstrated any prevention of restenosis after angioplasty. However, recent clinical trials in postmyocardial infarction reported that ACE inhibitor therapy reduces recurrent myocardial infarction and prevents cardiac enlargement. Long-term prospective trials are currently being conducted to examine the effects of ACE inhibitor therapy on coronary ischemic events and coronary atherosclerosis, as evaluated by angiography or intravascular ultrasound, and the relationship between coronary events and ACE gene polymorphism.