Search

To study the association of renin gene polymorphism with essential hypertension in the Chinese population, 86 hypertensive and 107 normotensive subjects were enrolled from an epidemiologic survey. Leukocyte DNA was extracted and digested with Hind III and Bgl I restriction enzymes. Southern hybridization was done with digoxigenin-incorporated renin gene probes generated by polymerase chain reaction. The restriction fragments were detected by anti-digoxigenin antibody and enzyme methods. Two Hind III polymorphysms of the renin gene (8.7 kb and 6.2 kb) were identified. The allele frequences were 129(75%) and 43(25%), respectively, in hypertensives; they were 139(65%) and 75(35%), respectively, in normotensives (chi2 = 4.074, p = 0.044). The genotypes of 8.7/8.7,8.7/6.2 and 6.2/6.2 were significantly different between hypertensives and normotensives, being 45(52%), 39(45%), 2(3%) and 48(45%), 43(40%), and 16(15%), respectively (chi2 = 9.002, p = 0.11). The Bgl I polymorphism did not show a difference between hypertensives and normotensives. Thus, we conclude that the renin gene Hind III polymorphysm is associated with hypertension in this Chinese population.

Insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene has been postulated as a risk factor for coronary heart disease. We conducted a case-control study of 271 Chinese, including 114 subjects with coronary artery disease (CAD), 42 with non-CAD and 115 apparently normal controls to examine the association of I/D polymorphism and CAD. The genotypes were identified by polymerase chain reaction and the plasma ACE activity was assayed by spectrophotometry. The allele and genotype frequencies were not different among the CAD, non-CAD and apparently normal groups (p = 0.42 and 0.63). Plasma ACE activity was not different among the three groups (p = 0.32). The D-allele and DD genotype were not more prevalent in subjects with low risk CAD (p = 0.07 and 0.16) and subjects with myocardial infarction (p = 0.79 and p = 0.35). No association was found between I/D polymorphism and severity of CAD (p = 0.42 and 0.70). In conclusion, the deletion polymorphism of the ACE gene may not be an independent risk factor in the development of CAD or myocardial infarction in this Chinese population. The unique or synergistic effect of other genes needs further study.

To examine the association between insertion/deletion (I/D) polymorphism of the angiotensin converting enzyme (ACE) gene and essential hypertension in a Chinese population, a case-control study was conducted using 157 hypertensive and 115 normotensive subjects. The I/D polymorphism of the ACE gene was identified by polymerase chain reaction. Plasma ACE activity was determined using spectrophotometry. The difference of allele frequencies between normotensives and hypertensives was statistically significant (chi 2 = 4.467, P = .035), while the genotype distribution was not different between normotensive and hypertensive subjects (chi 2 = 3.954, P = .138). Plasma ACE activity was highest in the DD genotype, followed by the ID genotype, and the lowest in the II genotype (P = .0001 in normotensives and P = .163 in hypertensives, respectively). Thus, we conclude that the ACE gene polymorphism is not associated with essential hypertension in this Chinese population, but plasma ACE activity is genetically determined in the normotensive Chinese.