alpha-adducin and angiotensin I-converting enzyme polymorphisms in essential hypertension

Citation
Cj. Clark et al., alpha-adducin and angiotensin I-converting enzyme polymorphisms in essential hypertension, HYPERTENSIO, 36(6), 2000, pp. 990-994
Citations number
28
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
HYPERTENSION
ISSN journal
0194911X → ACNP
Volume
36
Issue
6
Year of publication
2000
Pages
990 - 994
Database
ISI
SICI code
0194-911X(200012)36:6<990:AAAIEP>2.0.ZU;2-E
Abstract
This study focused on two genes that have previously been implicated in hyp ertension and may influence renal sodium handling, adducin, and angiotensin I-converting enzyme (ACE). We compared their polymorphic frequencies and i nteraction in patients with essential hypertension (n=128) and individually age- and gender-matched normotensive control subjects. The a-adducin G460W polymorphism was genotyped by DNA amplification and restriction digestion. The ACE VD polymorphism was assayed by a triple-primer method, with a "nes ted" polymerase chain reaction primer situated completely within the insert ion sequence of the I allele. The distributions of genotypes and alleles fo r the two polymorphisms were not significantly different between the case a nd control populations, and the cross-classification of cases by alpha -add ucin and ACE genotype gave a distribution similar to that of control subjec ts. We have previously reported that the distributions of genotypes for two linked polymorphisms in the aldosterone synthase gene (one in the steroido genic factor-1 [SF-1] binding site and the other an intronic conversion [IC ]) were significantly different between this cohort of essential hypertensi ves and matched control subjects. The cross-classification of cases by ;alp ha -adducin and SE-1, alpha -adducin and IC, ACE and SE-1, and ACE and IC g enotype gave a distribution similar to that of control subjects. Hence, no evidence was found to suggest an association between either the alpha -addu cin G460W or the ACE I/D polymorphism and hypertension in a careful case-co ntrol study. Furthermore, the ar-adducin G460W, ACE I/D, and aldosterone sy nthase SF-1 and IC polymorphisms do not appear to interact in our hypertens ive population.