Vol 11, No 2 (2007)
Original paper
Published online: 2007-05-18
Influence of interaction between AGT G-6A, ACE D/I and AGTR1 A1166C gene polymorphisms on blood pressure and arterial stiffness
Nadciśnienie tętnicze 2007;11(2):95-105.
Abstract
Background In a population-based approach we investigated whether polymorphisms in the genes encoding AGT
(G-6A), ACE (D/I) and AGTR1 (A1166C), alone or in combination, affected blood pressure and arterial stiffness
parameters.
Materials and methods We randomly recruited 52 families (82 parents and 103 offspring). Peripheral pressures were derived from conventional (SBPP, systolic blood pressure, DBPP, diastolic blood pressure, PPP pulse pressure) and 24h-ambulatory BP measurements (SBPA, DBPA, PPA), respectively. Central pressures (SBPC, DBPC, PPC), augmentation pressure (AG), peripheral (AIxP) and central (AIxC) augmentation indexes were assessed by pulse wave analysis. Polymorphisms of selected genes of the RAA system were detected in all participants.
Results In single gene analyzes, significant findings were revealed for ACE D/I polymorphism with respect to SBPA, SBPC, PPA and PPC. In further analyzes, the interactions between D/I ACE and A1166C AGTR1 gene polymorphisms reached statistically significant values with regard to SBPP (p = 0.02), SBPA (p = 0.03), SBPC (p = 0.03), PPP (p = 0.008), PPA (p = 0.02) and PPC (p = 0.007). In the analyzed population, for AGTR1 C allele carriers, SBPC was 7.5 mm Hg (p = 0.0005), PPP 7.7 mm Hg (p = 0.003), PPA 3.0 mm Hg (p = 0.09) and PPC 8.4 mm Hg (p = 0.0007) higher for ACE II homozygotes in comparison to DD homozygotes. For AGTR1 C allele carriers, with respect to arterial wall stiffness parameters, AG was 3.7 mm Hg (p = 0.004), AIxP 7.1% (p = 0.07) and AIxC 5.7% (p = 0.03) higher for ACE II homozygotes, as compared to DD homozygotes.
Conclusions The interactions between D/I polymorphism of the ACE gene and A1166C polymorphism of the AGTR1 gene revealing joint negative effect of ACE I allele and AGTR1 C allele, with respect to blood pressure and arterial stiffness.
Materials and methods We randomly recruited 52 families (82 parents and 103 offspring). Peripheral pressures were derived from conventional (SBPP, systolic blood pressure, DBPP, diastolic blood pressure, PPP pulse pressure) and 24h-ambulatory BP measurements (SBPA, DBPA, PPA), respectively. Central pressures (SBPC, DBPC, PPC), augmentation pressure (AG), peripheral (AIxP) and central (AIxC) augmentation indexes were assessed by pulse wave analysis. Polymorphisms of selected genes of the RAA system were detected in all participants.
Results In single gene analyzes, significant findings were revealed for ACE D/I polymorphism with respect to SBPA, SBPC, PPA and PPC. In further analyzes, the interactions between D/I ACE and A1166C AGTR1 gene polymorphisms reached statistically significant values with regard to SBPP (p = 0.02), SBPA (p = 0.03), SBPC (p = 0.03), PPP (p = 0.008), PPA (p = 0.02) and PPC (p = 0.007). In the analyzed population, for AGTR1 C allele carriers, SBPC was 7.5 mm Hg (p = 0.0005), PPP 7.7 mm Hg (p = 0.003), PPA 3.0 mm Hg (p = 0.09) and PPC 8.4 mm Hg (p = 0.0007) higher for ACE II homozygotes in comparison to DD homozygotes. For AGTR1 C allele carriers, with respect to arterial wall stiffness parameters, AG was 3.7 mm Hg (p = 0.004), AIxP 7.1% (p = 0.07) and AIxC 5.7% (p = 0.03) higher for ACE II homozygotes, as compared to DD homozygotes.
Conclusions The interactions between D/I polymorphism of the ACE gene and A1166C polymorphism of the AGTR1 gene revealing joint negative effect of ACE I allele and AGTR1 C allele, with respect to blood pressure and arterial stiffness.
Keywords: D/I polymorphismA1166C polymorphismarterial pressurearterial stiffness