Background. This study examined the effects of psychological stress on platelet α2-adrenergic receptor (α2-AR) binding sites in relation to stress-induced anxiety and changes in the inflammatory response system (IRS).
Methods. The maximum number of binding sites (Bmax) and their affinity (Kd) for [3H]-rauwolscine, a selective α2-AR antagonist, and the stimulated production of tumor necrosis factor-α (TNFα), the Th1-like cytokine, interferon-γ (IFNγ), and the Th2-like cytokines, interleukin-10 (IL-10) and IL-5, were measured in 35 university students a few weeks before (baseline) as well as on the day before a difficult, oral examination (stress condition). The State-Trait-Anxiety Inventory (STAI)- was recorded during both conditions. The Minnesota Multiphase Personality Inventory (MMPI-2TM) was used to assess psychasthenia (Scale 7).
Results. Academic examination stress induced a significant increase in α2-AR density in students whose STAI scores increased in the stress period, in female students and in students who scored higher on psychasthenia. There were significant and positive correlations between stress-induced anxiety and changes in α2-AR density. Stress-induced anxiety was accompanied by a pro-inflammatory and Th1-like response, i.e. increased IFNγ and TNFα production. The stress-induced changes in platelet α2-AR density were significantly and positively related to the production of TNFα, IL-10 and IL-5 and negatively to that of IFNγ.
Conclusions. Subchronic psychological stress in humans induces increased α2-AR density, which is related to stress-induced anxiety, an anxiety-prone constitution and female sex. Increased α2-AR density is accompanied by a Th2-like response and increased TNFα production. The results suggest that: (i) α2-AR density is sensitive to graded differences in stress-induced anxiety; and (ii) psychological stress is accompanied by intertwined responses in the catecholaminergic system, such as α2-ARs, and the IRS, such as Th1/Th2-like functions and the production of TNFα.