Angiotensin-converting-enzyme I/D polymorphism and angiotensinogen M235T polymorphism in cerebrovascular pathology

The aim of the present study is to evaluate the frequency of the angiotensi n I converting enzyme (ACE) gene polymorphism (I/D) and the angiotensinogen (AGT) gene polymorphism (M23 5T) in patients with cerebrovascular disorder s. Angiotensinogen gene encodes for angiotensinogen, which is the specific sub strate of renin to produce Angiotensin I. This gene maps on chromosome 1q42 -43 near the renin gene (Davis GK et al, 1997). There is evidence that conc entration of plasma angiotensinogen correlates with blood pressure and ther e are data suggesting that molecular variants of this gene might be causall y implicated in the pathogenesis of essential hypertension (Jeunemaitre X e t al 1992). The T235 polymorphism of AGT has been postulated as a risk fact or not only for hypertension but also for myocardial infarction (Frossard P M et al, 1998). ACE gene is located on chromosome 17q23, encodes the enzyme involved in the conversion of angiotensin I to angiotensin II and inactiva tes bradykinin. An Insertion/Deletion (VD) polymorphism has been detected a t intron 16 of this gene and since then there have been many reports studyi ng the relation between ACE genotype and risk for different cardiovascular diseases (Rigat B et al, 1990). As a component of the renin-angiotensin sys tem with a major influence in salt and water homeostasis and the maintenanc e of vascular tissue, a genetically determined overactivity of the renin-an giotensin system may influence blood pressure and also heart and vascular t issue growth. For this reason we have decided to investigate the relation b etween these molecular variants of both genes and different cerebrovascular disorders.