The model of immobilization stress with aperiodic foot shock (FS) was used to study the effect of a prolonged emotional stress on the functional condition of cortical and subcortical structures (hypothalamic and reticular structures in particular) in EEG activity and to elucidate their role in the development of endocrine and hypertensive reactions. It is shown that the development of hypertensive reactions in animals is stipulated by dynamic changes in the functional condition of the CNS, particularly in the hypothalamic neuroendocrinal control mechanism and reticular formation of the midbrain, which can be conditionally subdivided into 3 stages. The first is characterized by the emergence of short-time cycles of the hypersynchronized activity of slow waves in the cortical and subcortical mechanism, which is accompanied by adaptive hormonal secretion and transient effects of vascular reactions to FS; in the meantime neither neuroendocrinal nor blood pressure (BP) self-regulation mechanisms are impaired. The second stage is characterized (3-4 days after the beginning of the exposure) by the development of 'persistent' excitation in the CNS and the stabilization of a high level of hormones in the blood. Vascular reactions to FS are extremely prolonged ones; in intervals between FS applications BP fails to return to initial values. The third stage (1 month after cessation of experiments) is characterized by normal background EEG-activity in cortical-subcortical structures, normal indices of hormonal homeostasis but high level of BP. In response to 'repeated' stress, on the first experimental day, prolonged hypersynchronization of slow waves in cortical-subcortical structures occurred while BP reactions to FS were also prolonged and high hormonal secretion was observed. The data obtained suggest the high reactivity of reticular-hypothalamic structures which determine primarily the characteristics of both vascular and hormonal reactions that could be understood to be due to the result of previous experience (the first stage of stress).