Hypertension is closely linked to ischaemic stroke (IS) and atherosclerosis, but there are no studies correlating the candidate hypertensive gene, namely angiotensin converting enzyme (ACE) and adducin 1 (ADD1) with magnetic resonance angiographic (MRA) abnormality, therefore this study was undertaken.
The 460Trp variant of the alpha-adducin gene is unlikely to have a major effect on susceptibility to hypertension in the Japanese population studied, although the present study does not exclude the involvement of alpha-adducin in the pathogenesis of hypertension.
We studied the risk of stroke, coronary heart disease (CHD), and myocardial infarction (MI) associated with the alpha-adducin variant and examined the extent to which this risk is modified by the presence of hypertension.
The specific function of DNA methylation in regulating the expression of AH-related genes at promoter site was described for hydroxysteroid (11-beta) dehydrogenase 2 (HSD11B2), somatic angiotensin converting enzyme (sACE), Na+/K+/2Cl- cotransporter 1 (NKCC1), angiotensinogen (AGT), α-adducin (ADD1), and for other crucial genes in endocrine hypertension.
The ADD1Gly460Trp polymorphism is significantly associated with an increased risk of coronary artery disease as well as blood pressure, indicating that ADD1 plays a role in the pathogenesis of coronary artery disease as well as hypertension.
The 1797T allele of the beta-adducin gene is associated with increased risk of hypertension in post-menopausal women and in users of oral contraceptives, particularly in the presence of the mutated alpha-adducin Trp allele.
Our overall results suggest null association of α-adducinG460T and GNB3 C825T polymorphisms with hypertension in Chinese but indicate local marginal significance of C825T, as a putative salt-sensitive switch, in southern Chinese.
In this study, 3 physiologically important candidate gene mutations (angiotensinogen A[-6], alpha-AdducinGly460Trp, and G-Protein beta(3)-subunit C825T) were examined for their association with hypertension status in a sample of 904 African Americans from Jackson, Mississippi.
However, we failed to detect a positive association between the Gly460Trp polymorphism of ADD-1 and hypertension in a small series of Japanese subjects.
Our case-control study and the following meta-analysis failed to provide evidence for the genetic association of alpha-adducin gene G460W polymorphism with hypertension.
Our results therefore provide no support for a role for the alpha-adducin variant in hypertension, at least in our severely affected Anglo-white group with strong family history of HT.
Furthermore the identification of genetic polymorphisms in the effectors involved in the pathophysiology of hypertension or in the response to anti-hypertensive drugs, such as the p22phox subunit of NADPH oxidase, alpha-adducin or adrenergic receptors, has promoted the prospective of both better understanding of hypertension and individualized strategies for its treatment.
The results of this population-based cohort study suggest that the ADD1 gene contributes to the risk of hypertension and increases mean common carotid IMT in patients with type 2 diabetes.
Our analysis shows that the 460Trp variant of the alpha-adducin polymorphism is probably associated with a sodium-sensitive form of hypertension, while the polymorphisms of the angiotensin II type 1 receptor gene and the -344C/T variant of the aldosterone synthase gene are not associated with this phenotype.