GENETIC PREDISPOSITION TO HYPERTENSION: FACTS AND CONTROVERSIES

G.E. DEGTIAROVA, M.V. KHAITOVYCH,, L.V NATRUS

Abstract


The review provides information about the causes of onset of essential hypertension in young people. The main pathogenetic aspects of the disease – an imbalance of the renin-angiotensin-aldosterone system and the interaction of the various systems of regulation of vascular tone – are described. Particular emphasis is put on the role of genetic predisposition, especially to the single nucleotide polymorphisms. Some of the candidate genes, which polymorphisms can lead to the clinical manifestations of hypertension, are described in details. Great association was found between variability of ACE, AGT, AGTR1, NOS3 genes and increased blood pressure. Analysis of the role of single nucleotide polymorphism in pathogenesis of essential hypertension leads to the conclusion that the disease has multigenic character. Study of only one single nucleotide polymorphism as predisposing to essential hypertension cannot be conclusive. That’s why only complex evaluation of different variable genes can give the answer about the endogenous predisposition to disease. Moreover, the influence of environmental factors and their interaction with the genome polymorphism are presented. It cant be excluded that genetic factors do not play a key etiological role in the onset of the essential hypertension. Accumulated evidence suggests that genetic background only causes individual susceptibility to development of multifactor diseases such as essential hypertension. Great importance is put on trigger factors such as obesity, salt and alcohol intake, stress, metabolism disorders, low physical activity, and others. Only they under certain circumstances can initiate or accelerate the expression of candidate genes in phenotype. There is strong evidence that polymorphisms of genes may have a minimal effect on the risk of disease in patients with low influence of environmental factors or on the other hand, have the greatest impact in t

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