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.