Polymorphisms of the insertion / deletion ACE and M235T AGT genes and hypertension: surprising new findings and meta-analysis of data

Abstract

Background: Essential hypertension is a common, polygenic, complex disorder resulting from interaction of several genes with each other and with environmental factors such as obesity, dietary salt intake, and alcohol consumption. Since the underlying genetic pathways remain elusive, currently most studies focus on the genes coding for proteins that regulate blood pressure as their physiological role makes them prime suspects.

Polymorphisms of angiotensinogen and angiotensin-converting enzyme associated with lower extremity arterial disease in the Health, Aging and Body Composition study

“…The unbalanced vascular tones increase the arterial stiffness and, consequently, increase the risk of development of lower extremity arterial disease (LEAD) or other vascular diseases. Previous reports on the association of essential hypertension [12][13][14] and cardiovascular diseases 15,16 with G-6A, T174M, M235T and ACE are inconsistent, possibly due to small sample size or unrecognized confounders or effect modifiers. In addition, the relationship between RAS genes and LEAD in Europeans and Asians [17][18][19] is also inconsistent.…”

Recent Trends in Hypertension Genetics Research

“…DD Genotype individuals would have the highest ACE serum concentrations (Sayed et al, 2004;Mondry et al, 2005) and it is estimated that allele D would contribute with approximately half the variation of ACE plasma levels (O'Donnell et al, 1998). Significant gender differences were also reported in ACE I/D polymorphism.…”

Polymorphism of RAS in Patients with AT1-AA Mediated Steroid Refractory Acute Rejection

“…The angiotensin converting enzyme (ACE) gene displays an insertion/deletion polymorphism in intron 16, and homozygosity of the deletion allele is known to be associated with higher serum ACE levels [24]. The DD genotype of ACE gene is a risk factor for the progression of chronic renal failure in IgA nephropathy [25].…”