In humans, the ACE activity is partly under genetic control. It is suggested that about half of the interindividual difference in ACE levels may be accounted for its polymorphism (19, 20) . It is reported that mean ACE levels were lowest for II homozygotes, highest for DD homozygotes, and intermediate for ID heterozygotes (18, 21) . Danser et al. explained the higher ACE levels observed in subjects with D allele than those with the II genotype by the sequence harbored in the insert of ACE gene. This sequence was said to be very similar to a silencer element (22) . But it is not clear whether increased levels of ACE actually affects the levels of angiotenisn II because the renin-angiotensin system is regulated by feedback mechanism (22) .