AIM: To determine the role of neurohumoral dysfunction and overweight in a clinical course of arterial hypertension (AH). MATERIAL AND METHODS: 200 participants of the study aged 30-60 years with AH degree I-II with low, moderate and high overall cardiovascular risk and mean disease duration 11.1 +/- 9.5 years were examined for body mass index, levels of leptin, soluble leptin receptor, insulin, serotonin and adrenoreactivity. RESULTS: Neurohumoral dysfunction correlated with body mass index. It manifested with elevation of insulin and leptin levels, sympathetic hyperactivity and a decrease of serotonin. CONCLUSION: One of the mechanisms forming and sustaining AH in patients with overweight is leptin-dependent sympathetic hyperactivity while serotonin system activation is more important for patients with normal body weight. Hypertensive patients with obesity demonstrate insulin-dependent hyperleptinemia.
AIM: To determine the role of neurohumoral dysfunction and overweight in a clinical course of arterial hypertension (AH). MATERIAL AND METHODS: 200 participants of the study aged 30-60 years with AH degree I-II with low, moderate and high overall cardiovascular risk and mean disease duration 11.1 +/- 9.5 years were examined for body mass index, levels of leptin, soluble leptin receptor, insulin, serotonin and adrenoreactivity. RESULTS: Neurohumoral dysfunction correlated with body mass index. It manifested with elevation of insulin and leptin levels, sympathetic hyperactivity and a decrease of serotonin. CONCLUSION: One of the mechanisms forming and sustaining AH in patients with overweight is leptin-dependent sympathetic hyperactivity while serotonin system activation is more important for patients with normal body weight. Hypertensive patients with obesity demonstrate insulin-dependent hyperleptinemia.