PLASMINOGEN-ACTIVATOR INHIBITOR-1 AND ANGIOTENSIN-I-CONVERTING-ENZYMEGENE POLYMORPHISM IN PATIENTS WITH HYPERTENSION

Deletion polymorphism of angiotensin I-converting enzyme (ACE) gene ha s been reported to be an independent risk factor for myocardial infarc tion. Plasminogen activator inhibitor-1 (PAI-1) was proposed to be a l ink between the renin-angiotensin system and thrombotic risk. This stu dy was undertaken to investigate the possible association between the insertion/deletion (I/D) polymorphism of the ACE gene and plasma PAI-1 levels in 160 patients with mild-to-moderate hypertension. The I/D ge notypes were determined by polymerase chain reaction with oligonucleot ide primers flanking the polymorphic region in intron 16 of the ACE ge ne. Baseline levels of PAI-1 antigen and activity and tissue plasminog en activator (t-PA) antigen were determined in fasting morning plasma samples. It was found that patients with homozygote deletion (DD, n = 37) ACE genotype did not have significantly higher plasma levels of PA I-1 antigen (31.2 +/- 15.6 ng/mL v 28.4 +/- 15.1 ng/mL or 27.2 +/- 13. 2 ng/mL, P = .42), PAI-1 activity (16.2 +/- 10.6 IU/mL v 14.1 +/- 9.4 IU/mL or 15.0 +/- 9.9 IU/mL, P = .60), or t-PA antigen (14.6 +/- 6.0 n g/mL. v 13.4 +/- 4.9 ng/mL or 14.6 +/- 5.7 ng/mL, P = .40) as compared to those with heterozygote (DI, n = 67) or homozygote insertion (II, n = 56) genotypes. On multiple regression analysis, the ACE genotypes did not appear to be significant predictors for plasma PAI-1 levels an d t-PA antigen after adjustment with age, sex, body mass index, plasma triglyceride, cholesterol, and glucose. In conclusion, the results in dicated that the I/D polymorphism of the ACE gene was not related to p lasma PAI-1 levels in a Chinese population with hypertension. The ACE genotypes may not have a role in influencing the fibrinolysis in hyper tension. (C) 1998 American Journal of Hypertension, Ltd.