title: Association of in vivo β-adrenergic receptor sensitivity with inflammatory markers in healthy subjects.
abstract: 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.
authors.affiliation: Department of Psychiatry, University of California, San Diego, California, USA. frank.euteneuer@staff.uni-marburg.de
authors.forename: Frank
authors.initials: F
authors.lastname: Euteneuer
authors.forename: Paul J
authors.initials: PJ
authors.lastname: Mills
authors.forename: Winfried
authors.initials: W
authors.lastname: Rief
authors.forename: Michael G
authors.initials: MG
authors.lastname: Ziegler
authors.forename: Joel E
authors.initials: JE
authors.lastname: Dimsdale
mesh_terms: D000318:Adrenergic beta-Agonists / Q000008:administration & dosage; D000328:Adult; D000818:Animals; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism*; D003430:Cross-Sectional Studies; D005260:Female; D006304:Health Status; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000175:diagnosis*; D015850:Interleukin-6 / Q000097:blood; D007545:Isoproterenol / Q000008:administration & dosage; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D051381:Rats; D011943:Receptors, Adrenergic, beta / Q000502:physiology*; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000097:blood; D055815:Young Adult
chemical_list: D000318:Adrenergic beta-Agonists; D015415:Biomarkers; D015850:Interleukin-6; D011943:Receptors, Adrenergic, beta; D047888:Receptors, Tumor Necrosis Factor, Type I; D002097:C-Reactive Protein; D007545:Isoproterenol