Background: Essential hypertension is a widespread cardiovascular disorder. The hyperactivation of the sympathoadrenal system (SAS) is considered one of the primary pathogenetic mechanisms leading to the elevation of blood pressure and subsequent target organ damage. Objective: To evaluate the functional state of the sympathoadrenal system by assessing catecholamine levels in patients diagnosed with essential hypertension. Methods: The study included 78 patients with Stage II essential hypertension and a control group of 20 healthy individuals. The functional state of the SAS was evaluated by measuring plasma levels of epinephrine (adrenaline) and norepinephrine (noradrenaline) using high-performance liquid chromatography. Hemodynamic parameters, including systolic and diastolic blood pressure, and heart rate, were also recorded. Results: Patients with hypertension exhibited a significant increase in SAS activity. Plasma norepinephrine levels were significantly higher in the hypertensive group (412.5 ± 35.2 pg/mL) compared to the control group (265.4 ± 22.8 pg/mL, p < 0.05), indicating elevated sympathetic nervous system tone. Epinephrine levels were also increased (74.3 ± 8.1 pg/mL vs. 42.1 ± 5.4 pg/mL, p < 0.05). A strong positive correlation was found between plasma norepinephrine levels and both systolic blood pressure and heart rate. Conclusion: Essential hypertension is characterized by marked hyperactivation of the sympathoadrenal system. This sustained sympathetic overdrive contributes to the maintenance of high blood pressure and highlights the necessity of incorporating sympatholytic or neuromodulatory agents in the comprehensive management of these patients.

essential hypertension, sympathoadrenal system, catecholamines, norepinephrine, epinephrine, sympathetic nervous system.

Williams, B., Mancia, G., Spiering, W., Agabiti Rosei, E., Azizi, M., Burnier, M., ... & ESC Scientific Document Group. (2018). 2018 ESC/ESH Guidelines for the management of arterial hypertension. European Heart Journal, 39(33), 3021-3104.

Esler, M. (2014). Sympathetic nervous system moves toward center stage in cardiovascular medicine: from Thomas Willis to resistant hypertension. Hypertension, 63(2), 204-212.

Fisher, J. P., Young, C. N., & Fadel, P. J. (2009). Central sympathetic overactivity: maladies and mechanisms. Autonomic Neuroscience, 148(1-2), 5-15.

Grassi, G., Mark, A., & Esler, M. (2015). The sympathetic nervous system alterations in human hypertension. Circulation Research, 116(6), 976-990.

Guyenet, P. G. (2006). The sympathetic control of blood pressure. Nature Reviews Neuroscience, 7(4), 335-346.

Seravalle, G., & Grassi, G. (2022). Sympathetic nervous system, hypertension, and target organ damage. Current Hypertension Reports, 24(12), 653-662.

Tasić, I., & Kostić, S. (2018). The role of the sympathetic nervous system in the pathogenesis of essential hypertension. Arterial Hypertension, 22(3), 115-121.

Schlaich, M. P., Lambert, E., Kaye, D. M., Krozowski, Z., Campbell, D. J., Lambert, G., ... & Esler, M. D. (2004). Sympathetic augmentation in hypertension: role of nerve firing, norepinephrine reuptake, and angiotensin neuromodulation. Hypertension, 43(2), 169-175.

Oparil, S., Zaman, M. A., & Calhoun, D. A. (2003). Pathogenesis of hypertension. Annals of Internal Medicine, 139(9), 761-776.

Malpas, S. C. (2010). Sympathetic nervous system overactivity and its role in the development of cardiovascular disease. Physiological Reviews, 90(2), 513-557.

Parati, G., & Esler, M. (2012). The human sympathetic nervous system: its relevance in hypertension and heart failure. European Heart Journal, 33(9), 1058-1066.

Cohn, J. N. (1989). Sympathetic nervous system activity and the heart. American Journal of Hypertension, 2(12 Pt 2), 353S-356S.

DiBona, G. F., & Kopp, U. C. (1997). Neural control of renal function. Physiological Reviews, 77(1), 75-197.