Arterial properties in relation to genetic variation in α-adducin and the renin-angiotensin system in a White population

J. Seidlerová, J. A. Staessen, T. Nawrot, E. Brand, S. M. Brand-Herrmann, N. Casamassima, L. Citterio, S. Hasenkamp, T. Kuznetsova, Y. Li, P. Manunta, T. Richart, H. A. Struijker-Boudier, R. Fagard, J. Filipovskỳ

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Earlier studies have demonstrated the interaction between ADD1 and ACE in relation to arterial properties. We investigated whether arterial characteristics might also be related to interactions of ADD1 with other renin-angiotensin system genes. Using a family-based sampling frame, we randomly recruited 1064 Flemish subjects (mean age, 43.6 years; 50.4% women). By means of a wall-tracking ultrasound system, we measured the properties of the carotid, femoral and brachial arteries. In multivariate-adjusted analyses, we assessed the multiple gene effects of ADD1 (Gly460Trp), AGT (C-532T and G-6A) and AT1R (A1166C). In ADD1 Trp allele carriers, but not in ADD1 GlyGly homozygotes (P-value for interaction ≤0.014), femoral cross-sectional compliance was significantly higher (0.74 vs 0.65 mm2kPa-1; P=0.020) in carriers of the AT1R C allele than in AT1R AA homozygotes, with a similar trend for femoral distensibility (11.3 vs 10.2 × 10-3kPa-1; P=0.055). These associations were independent of potential confounding factors, including age. Family-based analyses confirmed these results. Brachial diameter (4.35 vs 4.18mm) and plasma renin activity (PRA) (0.23 vs 0.14 ng ml-1h-1) were increased (P=0.005) in AGT CG haplotype homozygotes compared with non-carriers, whereas the opposite was true for brachial distensibility (12.4 vs 14.4 × 10-3kPa-1; P=0.011). There was no interaction between AGT and any other gene in relation to the measured phenotypes. ADD1 and AT1R interactively determine the elastic properties of the femoral artery. There is a single-gene effect of the AGT promoter haplotypes on brachial properties and PRA.

Original languageEnglish
Pages (from-to)55-64
Number of pages10
JournalJournal of Human Hypertension
Volume23
Issue number1
DOIs
Publication statusPublished - 2009

Fingerprint

Renin-Angiotensin System
Homozygote
Arm
Femoral Artery
Thigh
Renin
Haplotypes
Population
Genes
Alleles
Brachial Artery
Age Factors
Carotid Arteries
Compliance
Multivariate Analysis
Phenotype
adducin

ASJC Scopus subject areas

  • Internal Medicine

Cite this

Seidlerová, J., Staessen, J. A., Nawrot, T., Brand, E., Brand-Herrmann, S. M., Casamassima, N., ... Filipovskỳ, J. (2009). Arterial properties in relation to genetic variation in α-adducin and the renin-angiotensin system in a White population. Journal of Human Hypertension, 23(1), 55-64. https://doi.org/10.1038/jhh.2008.113

Arterial properties in relation to genetic variation in α-adducin and the renin-angiotensin system in a White population. / Seidlerová, J.; Staessen, J. A.; Nawrot, T.; Brand, E.; Brand-Herrmann, S. M.; Casamassima, N.; Citterio, L.; Hasenkamp, S.; Kuznetsova, T.; Li, Y.; Manunta, P.; Richart, T.; Struijker-Boudier, H. A.; Fagard, R.; Filipovskỳ, J.

In: Journal of Human Hypertension, Vol. 23, No. 1, 2009, p. 55-64.

Research output: Contribution to journalArticle

Seidlerová, J, Staessen, JA, Nawrot, T, Brand, E, Brand-Herrmann, SM, Casamassima, N, Citterio, L, Hasenkamp, S, Kuznetsova, T, Li, Y, Manunta, P, Richart, T, Struijker-Boudier, HA, Fagard, R & Filipovskỳ, J 2009, 'Arterial properties in relation to genetic variation in α-adducin and the renin-angiotensin system in a White population', Journal of Human Hypertension, vol. 23, no. 1, pp. 55-64. https://doi.org/10.1038/jhh.2008.113
Seidlerová, J. ; Staessen, J. A. ; Nawrot, T. ; Brand, E. ; Brand-Herrmann, S. M. ; Casamassima, N. ; Citterio, L. ; Hasenkamp, S. ; Kuznetsova, T. ; Li, Y. ; Manunta, P. ; Richart, T. ; Struijker-Boudier, H. A. ; Fagard, R. ; Filipovskỳ, J. / Arterial properties in relation to genetic variation in α-adducin and the renin-angiotensin system in a White population. In: Journal of Human Hypertension. 2009 ; Vol. 23, No. 1. pp. 55-64.
@article{41db6762a8b8410db93c36f9f9fda6d5,
title = "Arterial properties in relation to genetic variation in α-adducin and the renin-angiotensin system in a White population",
abstract = "Earlier studies have demonstrated the interaction between ADD1 and ACE in relation to arterial properties. We investigated whether arterial characteristics might also be related to interactions of ADD1 with other renin-angiotensin system genes. Using a family-based sampling frame, we randomly recruited 1064 Flemish subjects (mean age, 43.6 years; 50.4{\%} women). By means of a wall-tracking ultrasound system, we measured the properties of the carotid, femoral and brachial arteries. In multivariate-adjusted analyses, we assessed the multiple gene effects of ADD1 (Gly460Trp), AGT (C-532T and G-6A) and AT1R (A1166C). In ADD1 Trp allele carriers, but not in ADD1 GlyGly homozygotes (P-value for interaction ≤0.014), femoral cross-sectional compliance was significantly higher (0.74 vs 0.65 mm2kPa-1; P=0.020) in carriers of the AT1R C allele than in AT1R AA homozygotes, with a similar trend for femoral distensibility (11.3 vs 10.2 × 10-3kPa-1; P=0.055). These associations were independent of potential confounding factors, including age. Family-based analyses confirmed these results. Brachial diameter (4.35 vs 4.18mm) and plasma renin activity (PRA) (0.23 vs 0.14 ng ml-1h-1) were increased (P=0.005) in AGT CG haplotype homozygotes compared with non-carriers, whereas the opposite was true for brachial distensibility (12.4 vs 14.4 × 10-3kPa-1; P=0.011). There was no interaction between AGT and any other gene in relation to the measured phenotypes. ADD1 and AT1R interactively determine the elastic properties of the femoral artery. There is a single-gene effect of the AGT promoter haplotypes on brachial properties and PRA.",
author = "J. Seidlerov{\'a} and Staessen, {J. A.} and T. Nawrot and E. Brand and Brand-Herrmann, {S. M.} and N. Casamassima and L. Citterio and S. Hasenkamp and T. Kuznetsova and Y. Li and P. Manunta and T. Richart and Struijker-Boudier, {H. A.} and R. Fagard and J. Filipovskỳ",
year = "2009",
doi = "10.1038/jhh.2008.113",
language = "English",
volume = "23",
pages = "55--64",
journal = "Journal of Human Hypertension",
issn = "0950-9240",
publisher = "Nature Publishing Group",
number = "1",

}

TY - JOUR

T1 - Arterial properties in relation to genetic variation in α-adducin and the renin-angiotensin system in a White population

AU - Seidlerová, J.

AU - Staessen, J. A.

AU - Nawrot, T.

AU - Brand, E.

AU - Brand-Herrmann, S. M.

AU - Casamassima, N.

AU - Citterio, L.

AU - Hasenkamp, S.

AU - Kuznetsova, T.

AU - Li, Y.

AU - Manunta, P.

AU - Richart, T.

AU - Struijker-Boudier, H. A.

AU - Fagard, R.

AU - Filipovskỳ, J.

PY - 2009

Y1 - 2009

N2 - Earlier studies have demonstrated the interaction between ADD1 and ACE in relation to arterial properties. We investigated whether arterial characteristics might also be related to interactions of ADD1 with other renin-angiotensin system genes. Using a family-based sampling frame, we randomly recruited 1064 Flemish subjects (mean age, 43.6 years; 50.4% women). By means of a wall-tracking ultrasound system, we measured the properties of the carotid, femoral and brachial arteries. In multivariate-adjusted analyses, we assessed the multiple gene effects of ADD1 (Gly460Trp), AGT (C-532T and G-6A) and AT1R (A1166C). In ADD1 Trp allele carriers, but not in ADD1 GlyGly homozygotes (P-value for interaction ≤0.014), femoral cross-sectional compliance was significantly higher (0.74 vs 0.65 mm2kPa-1; P=0.020) in carriers of the AT1R C allele than in AT1R AA homozygotes, with a similar trend for femoral distensibility (11.3 vs 10.2 × 10-3kPa-1; P=0.055). These associations were independent of potential confounding factors, including age. Family-based analyses confirmed these results. Brachial diameter (4.35 vs 4.18mm) and plasma renin activity (PRA) (0.23 vs 0.14 ng ml-1h-1) were increased (P=0.005) in AGT CG haplotype homozygotes compared with non-carriers, whereas the opposite was true for brachial distensibility (12.4 vs 14.4 × 10-3kPa-1; P=0.011). There was no interaction between AGT and any other gene in relation to the measured phenotypes. ADD1 and AT1R interactively determine the elastic properties of the femoral artery. There is a single-gene effect of the AGT promoter haplotypes on brachial properties and PRA.

AB - Earlier studies have demonstrated the interaction between ADD1 and ACE in relation to arterial properties. We investigated whether arterial characteristics might also be related to interactions of ADD1 with other renin-angiotensin system genes. Using a family-based sampling frame, we randomly recruited 1064 Flemish subjects (mean age, 43.6 years; 50.4% women). By means of a wall-tracking ultrasound system, we measured the properties of the carotid, femoral and brachial arteries. In multivariate-adjusted analyses, we assessed the multiple gene effects of ADD1 (Gly460Trp), AGT (C-532T and G-6A) and AT1R (A1166C). In ADD1 Trp allele carriers, but not in ADD1 GlyGly homozygotes (P-value for interaction ≤0.014), femoral cross-sectional compliance was significantly higher (0.74 vs 0.65 mm2kPa-1; P=0.020) in carriers of the AT1R C allele than in AT1R AA homozygotes, with a similar trend for femoral distensibility (11.3 vs 10.2 × 10-3kPa-1; P=0.055). These associations were independent of potential confounding factors, including age. Family-based analyses confirmed these results. Brachial diameter (4.35 vs 4.18mm) and plasma renin activity (PRA) (0.23 vs 0.14 ng ml-1h-1) were increased (P=0.005) in AGT CG haplotype homozygotes compared with non-carriers, whereas the opposite was true for brachial distensibility (12.4 vs 14.4 × 10-3kPa-1; P=0.011). There was no interaction between AGT and any other gene in relation to the measured phenotypes. ADD1 and AT1R interactively determine the elastic properties of the femoral artery. There is a single-gene effect of the AGT promoter haplotypes on brachial properties and PRA.

UR - http://www.scopus.com/inward/record.url?scp=57849168496&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=57849168496&partnerID=8YFLogxK

U2 - 10.1038/jhh.2008.113

DO - 10.1038/jhh.2008.113

M3 - Article

VL - 23

SP - 55

EP - 64

JO - Journal of Human Hypertension

JF - Journal of Human Hypertension

SN - 0950-9240

IS - 1

ER -