Parameters of daily blood pressure monitoring and serum levels of chemerin and nesfatin-1 in hypertensive patients with obesity

Abstract

Hypertension and obesity both are key cardiovascular risk factors. Known mechanisms of combined impact of obesity and other major cardiovascular risk factors are still not clear, but the data of epidemiological and clinical studies indicate the leading role of adipokines (a group of cytokines produced by adipose tissue) in the onset and progression of cardiovascular complications in obese patients [ 1]. In this aspect, the recently discovered adipokines, chemerin and nesfatin-1, are of interest. Chemerin is mainly synthesized in adipocytes and preadipocytes of perivascular and white adipose tissue, fibroblasts and platelets in the form of prochemerin. It has several active isoforms, which causes its pleiotropic effects, including prohypertensive action. A series of research has shown that chemerin has no effect on basal inflammatory status, but it promotes the production of nitric oxide and activates the PI3K-Akt-eNOS signaling pathway. The presence of endothelial dysfunction, which occurs in many cardiovascular diseases, increases the ability of chemerin to increase arterial tone, which causes the vasoconstrictor effect of this adipocytokine in the processes of vascular tone regulation and may contribute to the development of hypertension [2]. The main place of synthesis of nesfatin-1 is the hypothalamic nuclei. It is also synthesized in adipocytes, pancreatic beta cells, cells of gastric mucose and reproductive system. Nesfatin-1 is able to regulate the need for food, reduces the appetite and the amount of body fat produced, participates in the regulation of carbohydrate metabolism. Recent data suggests that nesfatin-1 is involved in the pathogenesis of hypertension, which is potentially implemented through the central system of melanocortin and oxytocin, and also expresses vasoconstrictor effects by suppressing the synthesis of nitric oxide