No abstract

Although agonist-induced desensitization of adrenergic receptors has been previously demonstrated, the regulation of adrenergic receptors during acute psychological stress has not been investigated in humans. We studied 30 first year medical students during final examination week and one month earlier. Platelet alpha 2 receptor binding was measured using 3H-yohimbine and leukocyte beta 2 receptor binding was measured with 125I-CYP (Iodocyanopindolol). During final examination week, platelet alpha 2-receptor binding affinity was significantly reduced, while levels of plasma catecholamines and reported anxiety were significantly increased, compared with the earlier period. Students showing the greatest increases in plasma norepinephrine and in reported anxiety also demonstrated the greatest reductions in alpha 2 receptor binding affinity. These data show that acute psychological stress can produce adrenergic receptor desensitization, possibly through increased levels of circulating norepinephrine.

We have previously demonstrated that the vasospastic attacks of Raynaud's disease can be induced despite blockade of efferent digital nerves and that feedback-induced vasodilation is mediated through a non-neural, beta-adrenergic mechanism. Here, we sought to determine the role of sympathetic activity, as measured by plasma epinephrine and norepinephrine, during finger temperature feedback and autogenic training. Thirty-one female patients with idiopathic Raynaud's disease were randomly assigned to receive finger temperature feedback or autogenic training over 28 days. Half of each group began and finished training during the follicular phase of the menstrual cycle, the other half during the luteal phase. During training, significant temperature elevations were shown by feedback patients but not by autogenic patients. There were no significant effects for norepinephrine and epinephrine for either group. Cycle phase did not interact with training effects or with catecholamines. These findings do not support the role of decreased sympathetic activation in behavioral treatments for Raynaud's disease.