Abstract

Objectives. Sympathetic activation has a role in the development of left ventricular hypertrophy (LVH). The presynaptic α2C-adrenoceptor inhibits the release of norepinephrine from sympathetic nerve terminals in the heart. A deletion polymorphism in the α2C-adrenoceptor (α2CDel322–325) generates a hypofunctional α2C-adrenoceptor, which may result in chronic adrenergic signalling. This study aimed to investigate whether the α2CDel322–325 polymorphism was associated with an increased prevalence of LVH in patients with systemic hypertension. Methods. Left ventricular mass was measured in 205 patients with systemic hypertension and 60 normal volunteers using a 1.5-T Philips MRI system. Genotyping was performed using a restriction fragment length polymorphism assay. Results. No significant difference was observed between the distribution of the α2CDel322–325 genotypes in hypertensive patients with LVH compared with those without LVH. Adjusting for confounding variables the odds ratio (OR) of being ins/del for the α2CDel322–325 and having LVH was 0.49 (95% CI 0.14–1.69, p = 0.256). Conclusions. These observations suggest that there is little evidence for an association between α2CDel322–325 polymorphism and an increased prevalence of LVH in patients with systemic hypertension.

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