Angiotensin converting enzyme (ACE), bound to the cell membrane of endothelial cells catalyzes the conversion of A I to A II and degradation of bradykinins. Circulating AII levels depend on AI levels and ACE activity. Major source of circulation ACE is the vascular endothelium. There are two distinct, functionally similar and interrelated RASs : tissue RAS and the circulatory RAS. The increase in tissue RAS activity and consequent increase in tissue A II level is predominantly influenced by ACE levels. Angiotensin converting enzyme gene (ACEG) polymorphism is thought to be associated with ischaemic and nonischaemic cardiovascular disease. The relatonship between ACEG polymorphism and hypertension is still controversial whereas the relation with left ventricular hypertrophy is well established. "The enhanced ACE activity caused by this gene polymorphism not only increases the A II generation, it's also associated with the blokadge of bradykinin-kallikrein system which stimulates the release of NO and other vasodilatory prostaglandins. The resulting endothelial dysfunction is a significant precursor to atherosclerosis. Subjects with DD genotype have an increased risk of ischaemic events attributed to high ACE and A II levels. The association between ACEG polymorphism and myocardial infarction, dilated / hypertrophic cardiomyopathy and post PTCA restenosis is still contraversial. Further studies confirming the ACEG or ACEG polymorphism as an independent risk factor in the physiologic and pathologic characteristics of cardiovascular disease would enable the clinicians to stratify patients into various risk categories and to institute appropriate risk factor modulations.
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