Abnormal responses to endothelial agonists in Raynaud's phenomenon and scleroderma

Objective. To further specify the site of vascular dysfunction in patients with Raynaud's phenomenon (RP) and scleroderma. Methods. Ten patients with RP and scleroderma and 11 healthy control subjects received brachial artery infusions of sodium nitroprusside, an endothelium independent vasodilator, bradykinin, and substance P while bilateral finger blood flow was measured with venous occlusion plethysmography. Results. Both groups showed vasodilation to sodium nitroprusside. However, in response to the endothelium dependent compounds bradykinin and substance P, the controls showed vasodilation, whereas the patients showed vasoconstriction. Conclusion. The vascular defect in RP and scleroderma does not lie at the site of the muscarinic receptor, but possibly in a distal signaling mechanism.