Aldosterone synthase (CYP11B2) -344 C/T polymorphism is related to antihypertensive response

Background: Our aim was to determine whether the aldosterone synthase (CYP11B2) -344 C/T polymorphism was associated with the blood pressure (BP)-lowering response to antihypertensive treatment. Methods: Patients with mild-to-moderate primary hypertension and left ventricular hypertrophy were random...

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Published inAmerican journal of hypertension Vol. 15; no. 5; pp. 389 - 393
Main Authors Kurland, Lisa, Melhus, Håkan, Karlsson, Julia, Kahan, Thomas, Malmqvist, Karin, Öhman, Peter, Nyström, Fredrik, Hägg, Anders, Lind, Lars
Format Journal Article
LanguageEnglish
Published Oxford Oxford University Press 01.05.2002
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Summary:Background: Our aim was to determine whether the aldosterone synthase (CYP11B2) -344 C/T polymorphism was associated with the blood pressure (BP)-lowering response to antihypertensive treatment. Methods: Patients with mild-to-moderate primary hypertension and left ventricular hypertrophy were randomized in a double-blind study to receive treatment with either the angiotensin II type 1 (AT1) receptor antagonist irbesartan (n = 43), or the β1-adrenergic receptor blocker atenolol (n = 43). The aldosterone synthase (CYP11B2) -344 C/T polymorphism was analyzed using solid-phase minisequencing and related to BP reduction after 3 months treatment. Serum aldosterone levels were measured. Results: After 3 months treatment the mean reductions in BP were similar for both treatment groups. When assessing the systolic BP reduction in the irbesartan group, patients with the TT variant had a more pronounced reduction (−21 ± 19 SD mm Hg, n = 17) than both the TC (−14 ± 18 mm Hg, n = 18) and CC (0 ± 17 mm Hg, n = 8) genotypes (P = .04). There was no association between this polymorphism and the diastolic BP response. The -344 C/T polymorphism was not associated with the BP response to atenolol. Nor was it related to the baseline serum aldosterone level. Conclusions: The aldosterone synthase -344 C/T polymorphism was related to the BP-lowering response in hypertensive patients treated with the AT1-receptor antagonist irbesartan.
Bibliography:ark:/67375/HXZ-NFR07VGZ-D
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This work has been supported by Uppsala County Association Against Heart and Lung Disease, the Department of Internal Medicine Uppsala University, Uppsala, Sweden; Karolinska Institutet, Stockholm, Sweden; the Swedish Heart–Lung Foundation, Bristol-Meyer Squibb Pharmaceutical Research Institute, Princeton, NJ; and Sanofi-Synthélabo, Paris, France.
istex:AE703A53EA14781D1E0DFF2E08E0983EEEB1350D
ISSN:0895-7061
1941-7225
1879-1905
DOI:10.1016/S0895-7061(02)02256-2