Traumatic spinal cord injury (SCI) leads to the immediate activation of the hypothalamus-pituitary-adrenal (HPA) axis. However, its proper function is impaired due to primary and secondary injury to the neural pathways of the sympathetic nervous system innervating the adrenal gland. Disruption of sympathetic innervation can strongly influence the expression of Angiotensin II receptors that are found at all levels of HPA axis. In this study, circulating Angiotensin II levels and the expression of Angiotensin II receptors within HPA axis after compression-induced SCI (40g weight for 15 min) at the Th9 spinal level was analyzed after 1, 3, 7, 14, 21 and 28 days. Elevated level of circulating Angiotensin II was observed during the first three days, and then it declined to the control values. The dynamic changes in the Angiotensin II receptor levels within the components of HPA axis (hypothalamic paraventricular nucleus, pituitary and adrenal gland) have been observed. They were accompanied by fluctuated changes of stress hormones such as corticotropin-releasing hormone, adrenocorticotropic hormone, corticosterone, etc. Compare to thoracic lower level, SCI induced at higher (Th1) spinal level decreased the receptor expression within the HPA axis as well as affected hormonal levels more markedly. We can conclude that the extent of sympathetic denervation of adrenal gland caused by traumatic SCI significantly affects neuroendocrine regulation and the expression of Angiotensin II receptors within the HPA axis. The study was supported by APVV-18-0163, APVV-22-0248 and VEGA No. 2/0123/23.