Abstract

PURPOSE: Angiotensin converting enzyme (ACE) I/D polymorphism influences ACE activity, with the D allele associated with higher angiotensin II production, which can have adverse effects on endothelial function through the promotion of vasoconstriction. Age is an independent risk factor for endothelial dysfunction, and postmenopausal women because estrogen deficiency affects their endothelial function. The present study was to investigate the trend of cardiovascular risk factors for endothelial function with aging in Han nationality women with ACE D/I polymorphism in Beijing. METHODS: A total of 391 females, age from 22 y to 75 y, were selected for analyzing the relationship between ACE I/D polymorphism and cardiovascular risk factors for endothelial function, (Ages 20-44: 120; Ages 45-59: 150; Ages 60-75: 121). Body composition, serum lipids metabolism, endothelial function, endothelium-derived relaxing factor and contracting factor were analyzed. RESULTS: The distribution characteristics of ACE I genotype and D genotype in han Chinese women in Beijing were as follows: Ages 20-44: 63.74% and 36.26%; Ages 45-59:67.33% and 32.67%; Ages 60-75:64.34% and 35.66%. There was no age associated with differential expression. Along with the women aging, DI/II genotype had higher TG level, higher chance of hyperglycemia and lower HDL level. The percentage of body fat and visceral fat significantly increased than DD type did. FMD, blood pressure, baPWV and IMT increased earlier and DBP abnormality rate, IMT, IMT thickening rate had more severe increases than DD type. The decrease of NO and NO/ET-1 and the increase of ET-1 and AngIIwere more significant compared with DD type. The interaction between age and ACE gene D/I polymorphisms could remarkably affect vascular endothelial function. CONCLUSIONS: There was no age associated with differential expression in ACE D/I polymorphism in Women of Han nationality in Beijing. The interaction between age and ACE D/I polymorphisms plays a key role in endothelial dysfunction, in which DI/II genotype is vulnerable to endothelial dysfunction and arteriosclerosis with aging.

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