Influence of Angiotensin II Type 1 Receptor Polymorphism on Aortic Stiffness in Never-Treated Hypertensive Patients

Author:

Benetos Athanase1,Topouchian Jirar1,Ricard Sylvain1,Gautier Sylvie1,Bonnardeaux Alain1,Asmar Roland1,Poirier Odile1,Soubrier Florent1,Safar Michel1,Cambien François1

Affiliation:

1. From INSERM U337, Broussais Hospital (A. Benetos, J.T., S.G., R.A., M.S.), INSERM SC7 (S.R., O.P., F.C.), and INSERM U36, College de France (A. Bonnardeaux, F.S.), Paris, France.

Abstract

Abstract Several clinical and experimental studies have suggested a significant role of angiotensin II in the development of alterations of small and large arteries. The present study was designed to assess the contribution of polymorphism (corresponding to an A 1166 →C transversion) of the angiotensin II type 1 receptor (AT 1 ) gene to aortic stiffness. One hundred thirty-four never-treated hypertensive patients were included in the study. Aortic distensibility was evaluated by measuring carotid-femoral pulse wave velocity. Age, systolic and diastolic pressure, and metabolic parameters were similar in the three genotypes. Pulse wave velocity was 11.4±2.5 m/s in AT 1 AA homozygotes, 12.5±3.2 m/s in AC heterozygotes, and 14.7±4.0 m/s in CC homozygotes ( P =.003, P <.001 after adjustment for age, blood pressure, and body mass index). Moreover, an interaction was found between AT 1 genotype and the ratio of total to high-density lipoprotein cholesterol in terms of the development of aortic stiffness. Thus, a positive correlation was observed between the ratio of total to high-density lipoprotein cholesterol and pulse wave velocity in AC and CC ( r =.42, P <.001) but not AA patients. These results suggest that the AT 1 gene is involved in the development of aortic stiffness in hypertensive patients and could modulate the effects of lipids on large arteries.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Internal Medicine

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