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Interplay between glycemia and the genetics of eNOS and ACE for the susceptibility to the onset and development of hypertension on the Portuguese population

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Hypertension is a multifactorial condition of genetic and environmental nature. In Portugal the mean prevalence of hypertension in the population is 45.5%. The aim of this study is to evaluate the contribution of anthropometric, physiological and genetic factors (eNOS and ACE) to the development of hypertension in a Portuguese population. A case-control study was conducted in a sample of 377 individuals, 243 hypertensives and 134 normotensives. The polymorphic analyses of intron 4 VNTR in the eNOS gene and the insertion/deletion (I/D) in ACE gene were performed by polymerase chain reaction (PCR). Higher body mass index (BMI) values, higher glycemia and HOMA -IR levels and the 4a allele of the eNOS gene were associated with hypertension. Among the hypertensive group, the allele 4a (eNOS) was associated with higher levels of HbA1c, and the D allele (ACE) with higher glycemia and HOMA-IR levels. Our results highlight the contribution of eNOS and ACE genes as importante players for development of hypertension in the Portuguese population. We believe that a combinatory clinical approach including the traditional anthropomorphic and physiological parameters together with target specific genetic analysis, can be more elucidative in establishing a susceptibility profile on multifactorial conditions as hypertension.
Highlights: Hypertensive Portuguese have higher levels of BMI, glycemia and HOMA-IR; 4a allele from eNOS is associated with hypertension in the Portuguese population; HbA1c levels are higher in hypertensive Portuguese carrying the 4a allele (eNOS); Glycemia and HOMA-IR levels are higher in Portuguese carrying the D allele (ECA); The interplay between eNOS and ECA genes is an important factor for hypertension.

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Glycemia eNOS ACE Hypertension Portugal Doenças Genéticas

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Citation

Gene Reports. 2021 Mar;22:100975. doi: 10.1016/j.genrep.2020.100975. Epub 2020 Dec 2.

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Elsevier

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