BLOCKADE OF VASOSPASTIC ATTACKS BY ALPHA(2)-ADRENERGIC BUT NOT ALPHA(1)-ADRENERGIC ANTAGONISTS IN IDIOPATHIC RAYNAUDS-DISEASE

Background Idiopathic Raynaud's disease is characterized by cold-induced digital vasospasms, but its origin has not been established: Previous research has shown that peripheral vascular alpha(2)-adrenergic receptors are hypersensitive to local cooling in these patients, but the role of alpha(1)-adrenergic receptors is not clear. Moreover, the role of adrenergic receptors in the production of actual vasospastic symptoms has not been investigated. Methods and Results We studied 23 patients with idiopathic Raynaud's disease who were screened using conservative criteria. They were randomly assigned to receive brachial artery infusions of alpha(1)-antagonist, an alpha(2)-antagonist, or both while vasospastic attacks were induced by cooling in the laboratory. Each patient's hands were photographed, and the number of attacks in the infused hand was compared with the number in the contralateral hand. The number of fingers (mean+/-SEM) with attacks in infused hands was yohimbine 0.3+/-0.3, prazosin 2.3+/-0.3, and both drugs 0.6+/-0.2. The difference between prazosin and the other two drug groups was significant (P<.001). Conclusions These findings demonstrate that activation of alpha(2)-adrenergic receptors but not alpha(1)-adrenergic receptors is necessary for the production of vasospastic attacks in idiopathic Raynaud's disease.