Endothelial nitric oxide synthase gene polymorphisms and cardiovascular damage in hypertensive subjects: an Italian case-control study

Daniela Colomba¹ , Giovanni Duro² , Salvatore Corrao¹ , Christiano Argano¹ , Tiziana Di Chiara¹ , Domenico Nuzzo² , Federica Pizzo² , Gaspare Parrinello¹ , Rosario Scaglione¹ and Giuseppe Licata¹

¹Department of Internal Medicine, University of Palermo, Italy

²Institute of Biomedicine and Molecular Immunology CNR, Palermo, Italy

author email corresponding author email

Immunity & Ageing 2008, 5:4doi:10.1186/1742-4933-5-4


Published:	29 May 2008

Abstract

Background

Nitric oxide (NO) synthesized by endothelial nitric oxide synthase (eNOS) plays an important role in regulation of endothelial function and in the control of blood pressure. However, the results from some studies on the association between three clinically relevant eNOS gene polymorphisms (G894T, T786C and intron 4b/a) and essential hypertension are unclear. We designed a case-control study to evaluate the influence of eNOS polymorphisms on target organ damage in 127 hypertensives and 67 normotensives. Clinical evaluation, biochemical parameters, Urinary Albumin Excretion (UAE) and echocardiogram were performed to characterize target organ damage. eNOS polymorphism were recognized by PCR method.

Results

The distribution of eNOS genotypes was similar in hypertensives and normotensives but 4aa was present in the 2.5% of hypertensives and completely absent in normotensives. Subjects with 4bb, G894T, and T786C genotypes showed an increased prevalence of target organ damage. Moreover prevalence of G894T and introne 4 variants was significantly higher in hypertensives than in normotensives both with cardiovascular damage. Logistic regression analysis didn't show any association between eNOS polymorphisms, Body Mass Index (BMI), hypertension, gender and cardiovascular damage. Only the age (OR 1.11; IC 95% 1.06–1.18) was predictive of cardiovascular damage in our population.

Conclusion

Our results seem to indicate a lack of association with eNOS variants and cardiovascular damage onset.