These findings raise the possibility that in some ethnic subgroups, variation in or near the ACE gene may contribute to the development, and severity, of hypertension.
No significant associations were detected between the ACE genotype and the development of hypertension, antihypertensive therapy required, progression rate of the disease, age of diagnosis and the antiproteinuric response to ACE-inhibition.
These data suggest that the I/D polymorphism of the ACE gene is associated with an early onset of hypertension and left ventricular hypertrophy in Japanese patients with essential hypertension.
The great variety of cardiovascular effects mediated by these vasoactive peptides and the efficacy of ACE inhibitors in the treatment of hypertension and heart failure emphasize the prominent role of ACE in the cardiovascular system.
Polymorphisms of the angiotensin converting enzyme (ACE) gene, although associated with left ventricular hypertrophy, do not appear to have a clear association with hypertension.
In protocol 2, ACE genotypes as well as microalbuminuria and renal hemodynamic parameters were investigated in 75 patients with EH with normal renal function and a strong family history of hypertension.
The results indicate that in normotensive subjects with a genetic predisposition to hypertension, ambulatory systolic blood pressure is related to the D allele of the ACE gene.
Therefore, we studied the association of the ACE gene I/D polymorphism with glucose intolerance and insulin resistance, and the contribution of this locus to genetic susceptibility to hypertension in non-insulin-dependent diabetic mellitus (NIDDM).
An I/D polymorphism in intron 16 of the gene coding for the angiotensin-converting enzyme (ACE) has been used to study the role of this gene in the aetiology of coronary atherosclerosis and hypertension.
Tissue angiotensin converting enzyme inhibition at a non-hypotensive dose almost completely prevented mortality from malignant hypertension and significantly reduced tissue injury in this model, implicating angiotensin II rather than high blood pressure as the principal 'vasculotoxic' agent in malignant hypertension.
To investigate the relation between the angiotensin converting enzyme gene polymorphism and extent of blood pressure elevation in arterial hypertension, taking into account the influence of cardiovascular risk factors.
A variant in the angiotensin-converting enzyme gene could not, initially, be convincingly associated with hypertension, but more recent analyses suggest an influence of the deletion allele on blood pressure in men, but apparently not in women.
Our results suggest a relationship between the prevalence of hypertension and the deletion polymorphism of the ACE gene in young type 1 diabetic patients, but we could not find an association between carotid artery IMT and ACE genotype in this population.
A significant association was detected between hypertension and the deletion/deletion (D/D) genotype of the ACE gene when the relation was adjusted for age, sex, and body mass index.
Considering cardiovascular diseases there is a number of genes involved in lipid metabolism (apolipoproteins, lipoprotein receptors, lipolytic enzymes), thrombosis/hemostasis (platelet receptors, pro- and anticoagulant proteins, fibrinogen, PAI's), hypertension (angiotensin converting enzyme, angiotensinogen) glucose metabolism (glucose transporters, enzymes) and obesity (hormones, receptors), that are interesting candidates for sophisticated genetic risk assessment.
Calcium antagonists can be used as alternatives to ACE inhibitors in patients with hypertension and concomitant diabetes mellitus and/or renal disease.
There is clear evidence that polymorphisms at the renin, angiotensinogen, and angiotensin-converting enzyme loci influence both blood pressure and hypertension.