Key result
The prevalence of the T235 variant of the angiotensinogen gene was not significantly higher in patients with essential hypertension compared to normotensive controls (60.2% vs 52.4%, P=0.22).
Why the study?
Is the T235 variant of the angiotensinogen gene associated with essential hypertension, plasma renin activity, or serum aldosterone levels in a Hispanic population?
Case-Control (n=126)
Is the T235 variant of the angiotensinogen gene associated with essential hypertension, plasma renin activity, or serum aldosterone levels in a Hispanic population?
Answers are grounded in this paper and cite their sources.
The T235 variant of the angiotensinogen gene is highly prevalent in the Chilean population but does not show a statistically significant association with essential hypertension in this small cohort.
BACKGROUND: The angiotensinogen gene has recently been linked to essential hypertension. A variant within this gene, encoding threonine rather than methionine at amino acid position 235, was associated with essential hypertension. However, results of new studies have not confirmed this association, suggesting that ethnic differences may explain the different results. OBJECTIVE: To evaluate whether the T235 variant is associated with a higher incidence of essential hypertension among Hispanics (a group that has scarcely been evaluated) and to determine whether T235 is associated with variations in the plasma renin activity or the serum aldosterone level. PATIENTS AND METHOD: We studied 64 patients with essential hypertension and 62 normotensives, matched for age and sex. We obtained samples for determinations of plasma renin activity, serum aldosterone level and genome DNA from all subjects. The genomic DNA was amplified using the polymerase chain reaction technique and digested by the restriction enzyme streptococcus faecalis (Sfa NI) which cuts M235 only, not T235. RESULTS: The patients with essential hypertension had a higher prevalence of the risk variant T235 (alleles 77/128 = 60.2%) than did the normotensive controls (alleles 65/124 = 52.4%), but the difference was not statistically significant (chi2=1.53, P=0.22). The plasma renin activity levels in hypertensives were not statistically different for homozygous T235, heterozygous and homozygous M235 (1.0 +/- 0.96, 2.0 +/- 2.25 and 1.55 +/- 1.49 ng/ml per h, respectively, P=0.5 1). However, when we considered those hypertensives with low plasma renin activity levels (< 1 ng/ml per h), we found a high prevalence (72.7%) of subjects homozygous for the T235 variant. We found no association between the T235 variant and the serum aldosterone levels in hypertensive and normotensive subjects. CONCLUSIONS: We demonstrated that there is a high prevalence of T235 variant in our Hispanic population. The slight difference between prevalences of T235 variant among hypertensive and normotensive subjects that we found was not statistically significant and did not permit us to establish an association between T235 variant and essential hypertension. We believe that only studying a larger cohort of subjects could show whether there is a quantitative effect of the T allele on plasma renin activity levels.
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Fardella et al. (1998) conducted a case-control in Essential hypertension (n=126). Essential hypertension vs. Normotensive controls was evaluated on Prevalence of the T235 variant allele (p=0.22). The prevalence of the T235 variant of the angiotensinogen gene was not significantly higher in patients with essential hypertension compared to normotensive controls (60.2% vs 52.4%, P=0.22).
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