Abstract

The article analyzes the results of conducted studies about the effect of catestatin on the development of arterial hypertension and type 2 diabetes mellitus, since hyperactivation of the sympathetic nervous system is a powerful pathogenetic mechanism of their progression. This paper considers the causes of increased secretion and release of catecholamines due to the activity of the sympathetic nervous system and its impact on the reduction of catestatin levels, which has an inhibitory effect blocking nicotinic acetylcholine receptors. Non-synonymous single nucleotide polymorphisms of the catestatin domain Gly364Ser, Pro370Leu, Arg374Gln, Gly367Val and the difference of their antiadrenergic activity in comparison with the wild type of catestatin are studied, the reasons of changes in the efficiency of catestatin alleles are determined. It is estimated the pathogenetic significance of low levels of catestatin in the development of hypertension through the mechanisms of impaired vasodilation and inhibition of catecholamines. The predictive significance of catestatin is based on decrease in its level in persons with hereditary predisposition to the development of arterial hypertension. The anti-inflammatory effect of catestatin determines its role in the pathogenesis of diseases accompanied by chronic inflammation, including type 2 diabetes mellitus and atherosclerosis. The role of catestatin in the regulation of glucose metabolism due to an insulin-like effect and inhibition of glucose secretion by hepatocytes, as well as improving glucose tolerance and insulin sensitivity, has been established. The perspectives of catestatin are determined as a potential biomarker of arterial hypertension and type 2 diabetes mellitus.

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