Objective: To explore the relationship of the ACE gene insertion/deletion (I/D) polymorphism and the rennin-angiotensin system in the pathogenesis of hypertension in OSAHS.
Method: Gene DNA was extracted from blood samples and amplified by polymerase chain reaction (PCR). The distribution of.the ACE gene I/D allele and genotypes were analyzed in 30 OSAHS with hypertension patients, 30 normotensive OSAHS patients and 30 healthy control group without cardiovascular diseases. The serum level of angiotensin II were also measured in all subjects by angiotensin II enzyme immunoassay kit.
Result: The frequency of II genotype and I allele were significantly higher in the OSAHS accompanied hypertension patients than those in the healthy controls (chi2=9.88, chi2=16.13, P<0.01, respectively) and in the normotensive OSAHS patients (chi2=5.67, P<0.05, chi2=8.61, P<0.01). The frequency of II genotype and I allele had no significantly different between the normotensive OSAHS patients and the healthy controls (P>0.05). The serum level of angiotensin II was significantly higher in both OSAHS patients with and without hypertension than that in the healthy control (t=3.66, t=3.23, respectively P<0.01). Whereas the serum level of angiotensin II have no significantly different in the OSAHS patients with and without hypertension (P>0.05).
Conclusion: These results indicate that the higher frequency of ACE gene I allele and genotype are closely associated with OSAHS patients accompanied hypertension. It is one of the important risk factors for the genesis of hypertension in OSAHS. The activity of rennin-angiotension system is higher in the OSAHS may have contribute to OSAHS-induced hypertension.