Association Between Polymorphisms of ADRBK1 Gene and Plasma Renin Activity in Hypertensive Patients: A Case-Control Study
نویسندگان
چکیده
BACKGROUND Renin is the first step of the RAS cascade, which is a major regulator of salt-volume homeostasis. Adrenergic beta receptor kinase 1 (ADRBK1) plays important roles in regulating blood pressure via the epithelial Na+ channel (ENaC), which plays an important role in Na+ reabsorption in the renal collecting duct. The present case-control study was designed to investigate the potential relationship between polymorphisms of ADRBK1 and plasma renin activity (PRA) in hypertension. MATERIAL AND METHODS We recruited 1831 hypertensive and 422 normotensive Han Chinese subjects. Sitting PRA (ng/mL/h) was measured using radioimmunoassay method. Hypertensive patients were classified into 4 renin categories via PRA quartile. Single-nucleotide polymorphisms (SNPs) of the ADRBK1 gene (rs1894111, rs4930416, rs7127431, rs12286664, and rs3730147) were identified via TaqMan polymerase chain reaction. RESULTS Comparison of the hypertensive group and the control group showed significant differences in distribution of genotypes and alleles of rs1894111 (P<0.05). Moreover, distribution of the dominant model (CC vs. CT+TT) in rs1894111 was lower in the hypertensive group than in the control group (P<0.05). Subjects were classified into 4 subgroups based on PRA quartile; the dominant model (CC vs. CT+TT) of rs1894111 was significantly lower in the quartile 1 group (the group with the lowest PRA) than in the control group (P<0.05). Logistic regression analysis demonstrated that the dominant model (CC vs. CT+TT) of rs1894111 was significantly different in the hypertensive group (OR=1.590, 95%CI=1.022-2.474, P<0.05), particularly in the quartile 1 group (OR=1.845, 95%CI=1.119-3.042, P<0.05), but not in the quartile 4 group. CONCLUSIONS The dominant model (CC vs. CT+TT) of rs1894111 polymorphism in the ADRBK1 gene might be associated with low-renin hypertension in Han Chinese.
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عنوان ژورنال:
دوره 22 شماره
صفحات -
تاریخ انتشار 2016