Genetic Influence on Baroreflex Sensitivity in Normotensive Young Men

Abstract

The dysfunction of baroreflex plays an important role in the pathogenesis of essential hypertension. Recent studies suggest that approximately 40% of the variation in baroreflex sensitivity (BRS) may be accounted for by genetic factors. However, only a few such genetic polymorphisms have been explicitly identified. A total of 182 normotensive young men were included in the study. They were tested for the occurrence of genotypes involving nine polymorphisms in six genes that have a role in the regulation of the cardiovascular system. BRS was calculated from the spontaneous fluctuation of systolic blood pressure (SBP) and heart interval, using a sequence method. BRS was negatively correlated with body mass index (BMI), SBP, and family history of hypertension. Univariate analysis revealed that BRS is significantly associated with three of the polymorphisms studied. At the polymorphism T-786C in the endothelial nitric oxide (NO) synthase (eNOS) gene, the subjects with TT genotype had lower BRS than subjects carrying either the TC or the CC genotype. At the polymorphism of C-344T in the aldosterone synthase gene (CYP11B2), subjects with the TT genotype had higher BRS as compared to those with CC. At the polymorphism of T-58C in the bradykinin B2 receptor (B2R) gene, subjects with CC genotype had lower BRS as compared to subjects with TT. A multivariable linear regression analysis indicated that 16% of the BRS variation could be explained by these three polymorphisms. Baroreflex function plays an important role in regulating blood pressure, both in the short term and in the long term. Three polymorphisms that are associated with the variation in BRS were identified in the eNOS, CYP11B2, and B2R genes, respectively; overall, they accounted for 16% of the BRS variation.