| Pregnancy induced hypertension (PIH) is one of severe diseases which badly endanger the health of pregnancy woman and fetus. Genetic factors appear to be important in pathogenesis of PIH, but the molecular basis of this genetic predisposition remains largely unknown. Vascular endothelial cells produce nitric oxide (NO), a vascular smooth muscle relaxing factor which plays an important role in the regulation of blood pressure and regional blood flow. NO is produced by endothelial nitric oxide synthase (eNOS) from Læ¢rginine, eNOS is only key synthase in this pathway. A large number of studies have shown that decreasing of NO is contributed to development of PIH. The mutation of eNOS gene resulted in decreasing of NO produce within PIH woman. So eNOS gene may be the candidate gene for PIH. A variant within exon 7 of eNOS gene: G to T conversion at nucleotide position 894 resulting in replacement of glutainic acid aspartic acide at condon 298 effects the stability of eNOS protein and results in decreasing of NO produce. Another variant within promoter of eNOS gene: T to C conversion at nucleotide position ?86 results in reducing promoter activity by ~5O% and impairs NO biosynthesis. To explore this two variants of eNOS gene, and to analysis the relationship between the eNOS 3 gene and PIH women in Chinese population, polymerase chain reaction 梤estriction fragment length polymorphism (PCR桼FLP) analysis was used to screen the variant G8941 in exon7 of eNOS gene in PIH and normotensive pregnancy women and random women and random people subjects; polymerase chain reaction single strand conformation polymorphism (PCR桽SCP) with PCR direct梥equencing analysis and polymerase chain reaction 梩emperature gradient gel electophersis (PCR桾GGE) analysis were used to screen the variant T?86C in promoter of eNOS gene in PIH and normotensive pregnancy women and random women subjects. The frequencies of variants (GT, TT) of exon 7 on 51 middle, server PIH women and 56 normotensive pregnancy women and 74 random women and 82 random peoples subjects were 35. 4%, 31. 1%, 26. 8%, 27. 5%, respectively. There were no statistical different in gene type of variants (GG, TI) of exon 7 among them (P0. 751). The I allele frequencies of exon 7 in middle, server PIH was 18. 3%, in normotensive pregnancy women was 15. 5%, in random women was 13. 4%, and in random peoples was 13. 7%. There were also no statistical different in I allele of eNOS gene exon7 among them (P0. 661). Another, the frequencies of variants (IC, CC) of promoter on 55 middle, server PJH women and 82 normotensive pregnancy women and 96 random women subjects were 19.8%, 15.9%, 20%, respectively. There were no statistical different in gene type of variants (IC, CC) of promoter of eNOS gene among them (P0. 951). The C allele frequencies of promoter in middle, server PIH was 10. 9%, in normotensive pregnancy women was 9.0%, and in random women was 11.8%. There were also no statistical different in C allele of promoter of eNOS gene among them (P0. 775). The results do not suggest that G894T in exon7 and I?86C in promoter of the eNOS gene are involved in development of PIH. Further work must to be done to seek evidence 4 for association be... |