Obesity, hypertension, and obesity-related hypertension are rapidly growing public health problems. Heightened sympathetic nerve activity is well-established observations in obesity and hypertension. Reduced energy expenditure and resting metabolic rate are predictive of weight gain, and the sympathetic nervous system participates in regulating energy balance through thermogenesis. The thermogenic effects of catecholamines in obesity have been mainly mediated via the β2 and β3-adrenergic receptors in humans. Further, β-adrenoceptors importantly influence vascular reactivity and insulin resistance. Obesity and hypertension have a strong genetic determinant. Genetic polymorphisms of the β- adrenoceptor gene have been shown to alter the function of β2- and β3-adrenoceptor subtype and thus to modify the response to sympathetic nerve activity (catecholamines). Among β2-adrenoceptor polymorphisms, Arg16Gly and Gln27Glu are considered the most functionally important in relation to obesity and hypertension. Genetic variations in the β3- adrenoceptor, such as the Try64Arg variant, are also associated with both obesity and hypertension. However, the precise relationships of the polymorphisms of β2- and β3-adrenoceptor genes with obesity and hypertension have been conflicting. Focusing on the relationships between the sympathetic nervous system and β2- and β3-adrenoceptor polymorphisms in obesity and hypertension might help to understanding these conflicting findings. The purpose of this article is to provide the current findings on the relationships between β-adrenoceptor polymorphisms, obesity, and hypertension including our own findings.