Exaggerated local hand sympathetic but not renin-angiotensin system activation in patients with primary Raynaud's phenomenon.

In Raynaud's disease (RD), an overactivity of sympathetic nervous system (SNS) was hypothesized but only indirect proofs were obtained. Complex interactions between the renin-angiotensin system (RAS) and SNS were reported without clear demonstrations of a RAS involvement. Recently, the use of ACE inhibitors and AT1 receptor antagonists in RD patients showed mixed results. The study of total and regional kinetics of tritiated noradrenaline (NA) and the measurements of local Angiotensin (Ang) I and II arterial-venous gradient were performed in 10 RD patients and 10 controls both in rest conditions and following a cold pressor test (CPT). Hand blood flow (HBF) was measured by strain-gauge plethysmography. Baseline HBF was slightly lower in patients than in controls, but during CPT, it significantly decreased only in RD patients (P < 0.01). Total (3H)-NA clearance and spillover were similar in the two groups throughout the study. On the contrary, baseline hand NA spillover was higher in RD patients than in controls and the difference further increased during CPT. Hand NA spillover was linearly related to HBF (P < 0.001). Arterial-venous Ang I and Ang II gradients were positive without difference between controls and patients throughout the study. In conclusion in RD patients, a pathological waste of NA from sympathetic nervous endings of the hand region, exaggerated by sympathetic stimulation, occurs but an enhanced local Ang II formation was not demonstrable.