Comorbid insomnia and arterial hypertension: Pathogenetic models and promising biomarkers

Abstract

The review describes the major mechanisms for the initiation and maintenance of comorbid insomnia and arterial hypertension based on the relevant pathogenetic scenarios of insomnia such as the concept of sympathetic activation, the neurobiological model of insomnia, and stress-diathesis model (or 3-P model). The clinical data are lacking, and available clinical studies indicate the association between blood pressure levels and the hyperactivation of the central nervous system during sleep, characterized by electroencephalographic β-activity, and with sleep latency. However, biologically active substances involved in “neurogenic inflammation” also play a significant role in homeostasis maintenance following the exposure to endogenous and exogenous stress factors. The functions of interleukin-6, gamma-aminobutyric acid, substance P, melatonin, serotonin and orexin in normal and pathological conditions indicate their contribution to the development of comorbid insomnia and hypertension. We emphasize the role of insomnia as a separate nosological unit, comorbid with hypertension, as well as the importance of research of molecular mechanisms underlying the association between insomnia and arterial hypertension aimed at identification of therapeutic targets and prognostic markers.