Genetic influences of β-adrenoceptor polymorphisms on arterial functional changes and cardiac remodeling in hypertensive patients

Three subtypes of S-adrenoceptor, 01, 02 and 63, are involved in the sympathetic nervous system, which plays an important role in the development of hypertension and hypertensive complications. These complications can include left ventricular hypertrophy and arterial stiffness, which are reported risk factors for cardiovascular diseases. We designed clinical trials to clarify the association between hypertensive complications and beta-adrenoceptor single nucleotide polymorphisms in essential hypertension. Using Taqman PCR methods, we detected five polymorphisms of three beta-adrenoceptors: Ser49Gly and Arg389Gly for the, beta(1)-adrenoceptor; Gly16Arg and Glu27GIn for the beta(2)-adrenoceptor; and Trp64Arg for the beta(3)-adrenoceptor. We included 300 subjects and measured pulse wave velocity, vasodilator response to hyperemia, left ventricular hypertrophy (by electrocardiogram and echocardiography), and cardiac enlargement (by chest Xray). We found that pulse wave velocity and nitroglycerin-induced hyperemia were both closely associated with the Ser49Gly polymorphism (p < 0.05), and Glu27GIn was found by both electrocardiogram and echocardiography to be significantly associated with left ventricular hypertrophy (p < 0.05). These data suggested that two polymorphisms of different beta-adrenoreceptor subtypes are the genetic influences on the development of arterial stiffness and left ventricular hypertrophy in essential hypertension.