Blockade of Vasospastic Attacks by α 2 -Adrenergic but Not α 1 -Adrenergic Antagonists in Idiopathic Raynaud’s Disease

Abstract

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 α ₂ -adrenergic receptors are hypersensitive to local cooling in these patients, but the role of α 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 an α ₁ -antagonist, an α 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 α ₂ -adrenergic receptors but not α ₁ -adrenergic receptors is necessary for the production of vasospastic attacks in idiopathic Raynaud’s disease.