OBJECTIVE: Several stress-related states and conditions that are considered to involve sympathetic overactivation are accompanied by increased circulating levels of inflammatory immune markers. Prolonged sympathetic overactivity involves increased stimulation of the β-adrenergic receptor (β-AR). Although prior research suggests that one mechanism by which sympathetic stimulation may facilitate inflammation is via β-AR activation, little work has focused on the relationship between circulating inflammatory immune markers and β-AR function within the human body (in vivo). We examined whether decreased β-AR sensitivity, an indicator of prolonged β-adrenergic overactivation and a physiological component of chronic stress, is related to elevated levels of inflammatory immune markers. METHODS: Ninety-three healthy participants aged 19 to 51 years underwent the chronotropic 25 dose isoproterenol test to determine in vivo β-AR function. Circulating levels of C-reactive protein, interleukin 6, and soluble tumor necrosis factor receptor 1 were determined. RESULTS: β-AR sensitivity was lower in people with higher C-reactive protein concentrations (r = 0.326, p = .003). That relationship remained significant after controlling for sociodemographic and health variables such as age, sex, ethnicity, body mass index, mean arterial blood pressure, heart rate, leisure-time exercise, and smoking status. No significant relationship was found between chronotropic 25 dose and interleukin 6 or soluble tumor necrosis factor receptor 1. CONCLUSIONS: This study demonstrates a link between in vivo β-adrenergic receptor function and selected circulating inflammatory markers (CRP) in humans. Future studies in specific disease states may be promising.
OBJECTIVE: Several stress-related states and conditions that are considered to involve sympathetic overactivation are accompanied by increased circulating levels of inflammatory immune markers. Prolonged sympathetic overactivity involves increased stimulation of the β-adrenergic receptor (β-AR). Although prior research suggests that one mechanism by which sympathetic stimulation may facilitate inflammation is via β-AR activation, little work has focused on the relationship between circulating inflammatory immune markers and β-AR function within the human body (in vivo). We examined whether decreased β-AR sensitivity, an indicator of prolonged β-adrenergic overactivation and a physiological component of chronic stress, is related to elevated levels of inflammatory immune markers. METHODS: Ninety-three healthy participants aged 19 to 51 years underwent the chronotropic 25 dose isoproterenol test to determine in vivo β-AR function. Circulating levels of C-reactive protein, interleukin 6, and soluble tumor necrosis factor receptor 1 were determined. RESULTS: β-AR sensitivity was lower in people with higher C-reactive protein concentrations (r = 0.326, p = .003). That relationship remained significant after controlling for sociodemographic and health variables such as age, sex, ethnicity, body mass index, mean arterial blood pressure, heart rate, leisure-time exercise, and smoking status. No significant relationship was found between chronotropic 25 dose and interleukin 6 or soluble tumor necrosis factor receptor 1. CONCLUSIONS: This study demonstrates a link between in vivo β-adrenergic receptor function and selected circulating inflammatory markers (CRP) in humans. Future studies in specific disease states may be promising.
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