Objactive Angiotensin II type 1 receptor is a important componment of renin angiotension system . Angiotensin converting enzyme (ACE), membrance binding protein, which can transform angiotensin I into angiotensin II. Ang II produces construction of vascular ang trachea by acting on smooth muscle. The clinical studies show that most patients of chronic pulmonary heart disease(CPHD) have the syndrom of high risk blood clot and angiotonia. In this study, we investigate the association between the ACE and AT1R gene polymorphisms with pulmonary heart disease on molecular level.Methods The ACE and AT1R genotype in the control group (40 subjects) and the study group(60 patients) is detected by the polymerase chain reaction (PCR).Results (1)In the control group, the distribution of the DD, II and ID genotypes of the ACE gene is 10. 0%, 47. 5% and 42. 5%;In the study group, the distribution of the DD, II and ID genotypes of the ACE gene is 20. 0%, 36. 7% and 43. 3%;There was no significant difference between two groups, I/D allele frequency and DD genotype /non DD genotype in control group do not significantly differ from the study group. (2)In the control group, the distribution of the AA, AC genotypes of the AT1R gene is 85. 0%,15. 0% . In the study group, the distribution of the AA, AC genotypes is 70. 3%, 29. 7%;There was also no difference of AT1R genetype and the allele frequency between the control group and the study group (P>0. 05). (3) In the female control group, the distribution of the AA, AC and CC genotypes of the AT1R gene is 87. 5%, 12. 5% and CC 0;In the male subgroup, the distribution of the AA, AC and CC genotypes of the AT1R gene is 83.3%,16. 7%, and 0;There was no significant difference between two subgroups, A/C allele frequency in control group do not significantly differ from the study group. (4)In the female subgroup of CPHD, the distribution of the AA.AC and CC genotypes of the AT1R gene is 70.4%, 29.6% and CC 0;In the male subgroup, the distribution of the AA,AC and CC genotypes of the AT1R gene is 69. 7%, 30. 3% and 0;These percentages in female subgroup significantly differ from the male subgroup, A/C allele frequency in female subgroup do not significantly differ form the male subgroup.(5) In the female control group, the distribution of the DD, II and ID genotypes of the ACE gene is 12. 5%, 50. 0% and 37.5%;In the male subgroup, the distribution of the DD, II and ID genotypes of the ACE gene is 8. 4%, 45. 8% and 45.8%;These percentages in the female subgroup do not significantlydiffer from the male subgroup, I/D allele frequency and DD genotype /non DD genotype in control group do not significantly differ from the study group. (6) In the female subgroup of CPHD, the distribution of the DD, II and ID genotypes of the ACE gene is 25. 9%, 48. 2% and 25.9%;In the male subgroup, the distribution of the DD, II and ID genotypes of the ACE gene is 15. 1%, 27. 3% and 57. 6%;These percentages in female subgroup significantly differ from the male subgroup, I/D allele frequency and DD genotype /non DD genotype in female subgroup do not significantly differ form the male subgroup. ?In 19 subjects of patients of CPHD accompanying with pulmonary embolism, the distribution of the AA, AC and CC genotypes of the AT1R gene is 84. 2%, 15.8% and 0. A/C allele frequency is 92. 1% and 7.9%. The percentages of AT1R genotypes is not significantly different between control group and subgroup, the A/C alleles frequency are significant association between the two groups. (§)In 19 subjects of patients of CPHD accompanying with pulmonary embolism, the distribution of the DD, II and ID genotypes of the ACE gene is 31. 6%, 26. 3%and 42. 1%. D/I allele frequency is 52.6% and 47.4%. The percentages of ACE genotypes is not significantly different in control group and subgroup, the percentages of DD genotype and non DD genotype, the I/D alleles frequency are significant association between the two groups. (9)The data of mean Hct is 0.521+0.155, 0. 528±0. 112 in the CPHD group, DD genotype subgroup. In the control group, the mean Hct is 0.483 + 0.056. There is not significantly different in control group comparing with CPHD group, DD genotype subgroup.Conclusion (D ACE I/D genotype polymorphism has a negative association with CPHD, DD genotype is not the risk factor of CPHD, but DD genotype is more prevalent in patients of CPHD. (2)In the female patients of CPDH, DD genotype is prevalent. DD genotype might be a risk factor in female patients of CPHD. (3) DD genotype is association with CPDH acompanying with pulmonary embolism. DD genotype and D allele may be the risk of this disease. (4) There was no association between AT1R gene polymorphism and CPDH, also pulmonary embolism. (5)AA and DD genotype is not association with the mean Hct of control group. |