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 in | American journal of hypertension Vol. 15; no. 5; pp. 389 - 393 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Oxford
Oxford University Press
01.05.2002
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Subjects | |
Online Access | Get full text |
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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. |
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Bibliography: | ark:/67375/HXZ-NFR07VGZ-D href:15_5_389.pdf 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 |