Vol 10, No 2 (2006)
Original paper
Published online: 2006-04-18
Influence of selected genetic polymorphisms of angiotensinogen, angiotensin-converting enzyme and type-1 angiotensin II receptor on arterial pressure and large artery stiffness parameters - depending on sodium intake
Nadciśnienie tętnicze 2006;10(2):99-110.
Abstract
Background In a population-based and family-based approach
we investigated, to what extent blood pressure and
large artery stiffness relate to the AGT G-6A, ACE D/I
and AGT1R A1166C gene polymorphisms, as well as the
interaction between genetic and environmental factors and
their joint influence on the aforementioned parameters.
Materials and methods We recruited 52 families (82 parents and 103 offspring). Peripheral pressures were derived from conventional and 24h-ambulatory blood pressure measurements, respectively. Central pressures and large artery stiffness parameters were assessed by pulse wave analysis. All participants collected a 24-h urine sample for the measurement of sodium excretion as well as blood sample for the evaluation of genetic analyses.
Results In single gene analyzes, significant findings were revealed for ACE D/I polymorphism with respect to 24h-ambulatory and central systolic (SBPA, SBPC) and pulse (PPA, PPC) pressures. In further analyzes, we found an interaction between ACE D/I genotype and 24-h urinary sodium excretion in relation to SBPC, conventional pulse pressure (PPP), PPC and augmentation pressure (AG). In the third tertile of the distribution of sodium excretion we observed significantly increased SBPC, PPP, PPA, PPC and AG in ACE II homozygotes compared to D allele carriers, which was not observed in first and second tertile.
Conclusions In the examined group, the interactions between D/I polymorphism of the ACE gene and daily sodium excretion in the urine were revealed, in relation to the parameters of blood pressure and arterial wall stiffness.The D allele of ACE gene showed a protective role in the group of subjects with high daily sodium intake.
Materials and methods We recruited 52 families (82 parents and 103 offspring). Peripheral pressures were derived from conventional and 24h-ambulatory blood pressure measurements, respectively. Central pressures and large artery stiffness parameters were assessed by pulse wave analysis. All participants collected a 24-h urine sample for the measurement of sodium excretion as well as blood sample for the evaluation of genetic analyses.
Results In single gene analyzes, significant findings were revealed for ACE D/I polymorphism with respect to 24h-ambulatory and central systolic (SBPA, SBPC) and pulse (PPA, PPC) pressures. In further analyzes, we found an interaction between ACE D/I genotype and 24-h urinary sodium excretion in relation to SBPC, conventional pulse pressure (PPP), PPC and augmentation pressure (AG). In the third tertile of the distribution of sodium excretion we observed significantly increased SBPC, PPP, PPA, PPC and AG in ACE II homozygotes compared to D allele carriers, which was not observed in first and second tertile.
Conclusions In the examined group, the interactions between D/I polymorphism of the ACE gene and daily sodium excretion in the urine were revealed, in relation to the parameters of blood pressure and arterial wall stiffness.The D allele of ACE gene showed a protective role in the group of subjects with high daily sodium intake.
Keywords: ACED/I polymorphismarterial pressurearterial stiffnesssodium intake