BACKGROUND: Sodium overload is related to the development of primary hypertension and its complications. METHODS: In 131 (65 female) treated hypertensives (average blood pressure 144/82 mmHg and duration of hypertension 11.7 years), we measured peripheral and central arterial pressures, peripheral (AIx(P)) and central (AIx(C1), AIx(C2)) augmentation indices, pulse-wave velocity (PWV) and daily urinary sodium excretion, and conducted genetic studies of ACE D/I and CYP11B2 C-344T polymorphisms. Proximal (FE(Li)) and distal (FDR(Na)) sodium reabsorption measurements were performed using endogenous lithium clearance. RESULTS: We found statistically significant interactions between FE(Li) and ACE D/I polymorphism with respect to AIx(C2) (P(INT) = 0.05) and between FE(Li) and CYP11B2 C-344T polymorphism with respect to AIx(C1) (P(INT) = 0.01), AIx(C2) (P(INT) = 0.04) and AIx(P) (P(INT) = 0.01). In the group of ACE I allele carriers compared with DD homozygotes, the AIx(C1) (154.1 vs 140.6%; p = 0.02), AIx(C2) (33.3 vs 26.9%; p = 0.02) and AIx(P) (94.6 vs 85.2%; p = 0.01) were higher in the subgroup with FE(Li) below the median value (FE(Li)1), but not in the subgroup with FE(Li) above the median value (FE(Li)2). In the group of CYP11B2 TT homozygotes compared with C allele carriers, we observed higher values of AIx(C1) (158.5 vs 146.4%; p = 0.03), AIx(C2) (36.0 vs 29.4%; p = 0.01) and AIx(P) (99.0 vs 88.7%; p = 0.005) in the FE(Li)1 but not the FE(Li)2 subgroup. Conclusions. In the population with assumed high dietary sodium intake and long-standing history of hypertension, the relation between proximal sodium reabsorption and the development of arterial stiffness depends on the genetic context of the selected genetic polymorphisms of the renin—angiotensin—aldosterone system, independent of blood pressure.
BACKGROUND:Sodium overload is related to the development of primary hypertension and its complications. METHODS: In 131 (65 female) treated hypertensives (average blood pressure 144/82 mmHg and duration of hypertension 11.7 years), we measured peripheral and central arterial pressures, peripheral (AIx(P)) and central (AIx(C1), AIx(C2)) augmentation indices, pulse-wave velocity (PWV) and daily urinary sodium excretion, and conducted genetic studies of ACE D/I and CYP11B2C-344T polymorphisms. Proximal (FE(Li)) and distal (FDR(Na)) sodium reabsorption measurements were performed using endogenous lithium clearance. RESULTS: We found statistically significant interactions between FE(Li) and ACE D/I polymorphism with respect to AIx(C2) (P(INT) = 0.05) and between FE(Li) and CYP11B2C-344T polymorphism with respect to AIx(C1) (P(INT) = 0.01), AIx(C2) (P(INT) = 0.04) and AIx(P) (P(INT) = 0.01). In the group of ACE I allele carriers compared with DD homozygotes, the AIx(C1) (154.1 vs 140.6%; p = 0.02), AIx(C2) (33.3 vs 26.9%; p = 0.02) and AIx(P) (94.6 vs 85.2%; p = 0.01) were higher in the subgroup with FE(Li) below the median value (FE(Li)1), but not in the subgroup with FE(Li) above the median value (FE(Li)2). In the group of CYP11B2 TT homozygotes compared with C allele carriers, we observed higher values of AIx(C1) (158.5 vs 146.4%; p = 0.03), AIx(C2) (36.0 vs 29.4%; p = 0.01) and AIx(P) (99.0 vs 88.7%; p = 0.005) in the FE(Li)1 but not the FE(Li)2 subgroup. Conclusions. In the population with assumed high dietary sodium intake and long-standing history of hypertension, the relation between proximal sodium reabsorption and the development of arterial stiffness depends on the genetic context of the selected genetic polymorphisms of the renin—angiotensin—aldosterone system, independent of blood pressure.