Effect of ACE gene I/D polymorphism on hypertension-related traits in french-canadian families

Abstract

Angiotensin-converting enzyme (ACE) gene is a well known blood pressure candidate gene as demonstrated by previous studies, where its insertion/deletion (I/D) polymorphism has been shown to be associated with hypertension and coronary artery disease, and plasma ACE concentrations have been found to be associated with plasma triglyceride and total cholesterol levels. The aim of this study was to determine the effect of the I/D polymorphism on hypertension-related traits in French-Canadian families. 125 French-Canadian families were selected on the basis of having at least one sib pair affected by early-onset (<55 years) hypertension and dislipidemia. From these, 542 individuals were genotyped for I/D marker and a sib pair linkage analysis (SIBPAL, from S.A.G.E. package) adapted to familial structures was performed for seventy hypertension-related traits. In this population, allelic frequency was: allele I = 42.5%, allele D = 57.5%. The genotypic distribution was: I/I = 17.7%, I/D = 49.6% and D/D = 32.7%. The linkage analysis was significant for NaLi countertransport (p=0.03) in male sib pairs, for plasma levels of vasopressin (p=0.002) and of glucose (p=0.007) in female sib pairs and of ANP (p=0.003) in mixte sib pairs. Microalbumin excretion (p=0.037) was significantly linked in hypertensive sib pairs, whereas volume of total body water (p=0.005) and of intracellular water (p=0.012) correlated with the marker in normotensive sib pairs. No significative effect of the Ace locus was found for the systolic or diastolic blood pressures, left ventricular hypertrophy, wake or sleep heart rates, BMI, cholesterol or triglyceride levels in neither hypertensive nor normotensive gender specific groups. In French-Canadian population, the effect of Ace gene I/D marker on hypertension-related traits varies depending on hypertension status and gender. Results of the present genetic study underline the importance of Ace locus in the pathogenesis of hypertension, with a distinct effect on some previously suggested linkages.