BACKGROUND: The human G-protein beta 3 subunit gene (GNB3) and some of its variants are known to be important genetic influences involved in essential hypertension (EH). Left ventricular hypertrophy (LVH) has long been thought to be an end point of EH, rather than a separate entity, though it is influenced by a unique set of hormonal, vascular and genetic factors. METHODS/MATERIALS: We carried out a retrospective, case-control study of a GNB3 825 C>T dimorphism among nationals from the United Arab Emirates (Emirati), an ethnic group characterized by no alcohol intake and no cigarette smoking, for putative correlations with EH and LVH. We investigated a sample population of 454 Emirati (231 men, 223 women) comprising groups of controls and patients with clinical diagnoses of LVH, based on echocardiographic and ECG criteria, and EH, based on blood pressure values. The GNB3 825 C>T genotypes were determined by PCR and restriction digestion. RESULTS: The distribution of genotypes was in Hardy-Weinberg equilibrium in all three subject groups. GNB3 T825 alleles demonstrated a strong association with LVH (OR = 2.22; 95% CI: 1.29-3.83 and P = 0.0002), but not with EH. CONCLUSIONS: GNB3 825 C>T is likely to be a significant risk factor for LVH but not for EH in the Emirati population, thereby strengthening the view that LVH is genetically a separate clinical entity.
BACKGROUND: The humanG-protein beta 3 subunit gene (GNB3) and some of its variants are known to be important genetic influences involved in essential hypertension (EH). Left ventricular hypertrophy (LVH) has long been thought to be an end point of EH, rather than a separate entity, though it is influenced by a unique set of hormonal, vascular and genetic factors. METHODS/MATERIALS: We carried out a retrospective, case-control study of a GNB3 825 C>T dimorphism among nationals from the United Arab Emirates (Emirati), an ethnic group characterized by no alcohol intake and no cigarette smoking, for putative correlations with EH and LVH. We investigated a sample population of 454 Emirati (231 men, 223 women) comprising groups of controls and patients with clinical diagnoses of LVH, based on echocardiographic and ECG criteria, and EH, based on blood pressure values. The GNB3 825 C>T genotypes were determined by PCR and restriction digestion. RESULTS: The distribution of genotypes was in Hardy-Weinberg equilibrium in all three subject groups. GNB3 T825 alleles demonstrated a strong association with LVH (OR = 2.22; 95% CI: 1.29-3.83 and P = 0.0002), but not with EH. CONCLUSIONS:GNB3 825 C>T is likely to be a significant risk factor for LVH but not for EH in the Emirati population, thereby strengthening the view that LVH is genetically a separate clinical entity.