Aldosterone synthase (CYP11B2) -344 C/T polymorphism is related to antihypertensive response: Results from the Swedish Irbesartan left ventricular hypertrophy investigation versus atenolol (SILVHIA) trial
2002 (English)In: American Journal of Hypertension, ISSN 0895-7061, Vol. 15, no 5, 389-393 p.Article in journal (Refereed) Published
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 ß1-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. © 2002 American Journal of Hypertension, Ltd.
Place, publisher, year, edition, pages
2002. Vol. 15, no 5, 389-393 p.
Aldosterone synthase, CYP11B2, Genetics, Hypertension, Treatment
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:liu:diva-47005DOI: 10.1016/S0895-7061(02)02256-2OAI: oai:DiVA.org:liu-47005DiVA: diva2:267901