PS 07-03 eNOS GENE POLYMORPHISMS IN SUDANESE PATIENTS WITH ESSENTIAL HYPERTENSION

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Abstract

Objective:

To investigate the association between 3 polymorphisms in Endothelial Nitric Oxide Synthase (eNOS) gene (Glu298Asp, VNTR intron 4 and T-786C) and Essential Hypertensiomsion (EH) in Sudanese patients.

Design and Method:

This is a Case-control study. 258 hypertensive patients from different hospitals in Khartoum and 149 age-matched controls with normal blood pressure were studied. Genomic DNA was extracted and the presence of the eNOS variant was determined by the Taqman SNP genotyping assay and by polymerase chain reaction–restriction fragment-length polymorphism (PCR-RFLP) analysis. Genotype and allele frequencies were compared between the 2 groups and a p value of < 0.05 was considered as statistically significant.

Results:

Homozygosity for the variation in the promotor T-786C existed similarly in cases and controls. However, when we assumed a dominant model of inheritance, the frequency of TC+CC in patients was significantly higher than in control subjects (50.4% and 39.5%, respectively, P = 0.034) with an odd ratio of 1.56. Genotyping of VNTR found a higher frequency of the variation aa in the controls than in patients (7.7% and 5.1% respectively) but the difference was not significant. Genotype distribution and allele frequency of Glu298Asp were similar between patients and controls. Neither dominant nor recessive models showed significant differences between the two groups. Surprisingly the T allele was found higher in controls than in patients but the difference was not significant (3.5% and 4.2% respectively).

Conclusions:

Our results indicated that variation in the Glu298Asp and VNTR in intron 4 of the eNOS gene was not associated with essential hypertension in Sudanese population. On the other hand, the polymorphism in the promotor region T-786C was found significantly higher in hypertensives if the dominant model was assumed. Further studies are required to confirm our results and characterize the molecular mechanisms by which T-786C is involved in EH.

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