The paper presents a current concept of the genesis of stress and adaptation with regard to new data on serotonin and its receptors. There is evidence that stress is transient hypoxia that results from dysfunction of smooth muscles (SM) in the microcirculatory bed (a pharmacological stage) with partial or complete dysfunction of the organ or system where dysfunction has occurred (a clinical stage). Impaired interaction of serotonin with GM serotonin receptors, which occurs with excess serotonin receptor ligands due to various stress factors, underlie the pharmacological and clinical manifestations of stress. The occurrence of transient hypoxia is followed by the activation of antistress (adaptive) processes in the organism with thrombocytic release of serotonin. In endogenous hyperserotoninemia, microcirculation improves, a hypoxic area ceases, and/or damaged and necrotic tissues localize. With this, endogenous serotonin-induced recovery of different organs is the essence of an adaptive process. Clinical and experimental evidence suggesting that exogenous serotonin administration just simulates an elevation in the concentration of endogenous serotonin as a material substrate of the human adaptive system.
