To investigate whether the variable efficacy in Raynaud's phenomenon of long-term oral ketanserin treatment might be related to variation in the sensitivity of 5-HT2 receptors to ketanserin, serotonin-induced platelet aggregation was measured in ten patients with Raynaud's phenomenon at various times after treatment with ketanserin. Platelet aggregation was completely inhibited 90 min after 40 mg ketanserin, but not 12-14 h after the last dose of 40 mg on the 31st day of continuous twice daily administration. However, 90 min after an additional dose of 40 mg, platelet aggregation was again completely inhibited. The present results indicate that ketanserin 40 mg b.d. does not continuously inhibit platelet 5-HT2 receptors in patients with Raynaud's phenomenon and suggest that more frequent intake might be more effective.

Summary:To investigate the role of the sympathetic System in Raynaud's phenomenon, which has not yet been elucidated, we measured the levels of norepinephrine, epinephrine and dopamine before, immediately and 30 min after the cold pressor test in plasma from 17 patients with primary, 6 with secondary RaynautTs phenomenon and 19 volunteers, matched for age and sex. Patients had significantly low baseline epinephrine (0.13 ± 0.02 vs 0.37 ± 0.04, nmol/1, p < 0.001, mean ± S. E.), but normal norepinephrine and dopamine (norepinephrine: 1.77 ± 0.16 and 2.06 + 0.18; dopamine: 0.10 ± 0.01 and 0.11 + 0.02, patients and controls).Immediately after the cold test norepinephrine significantly increased (p < 0.001) in patients (2.42 + 0.22) and controls (3.24 ± 0.28); epinephrine increased in patients (0.18 ± 0.02, p < 0.02); dopamine did not show any significant change (0.13 ± 0.01 and 0.13 ± 0.02, patients and controls).In the recovery period, while norepinephrine and epinephrine returned to baseline in both groups, dopamine increased in controls (0.21 + 0.04, p < 0.005) but remained unchanged in patients (0.11 ± 0.01).We conclude that there is no sympathetic overactivity in Raynaud's phenomenon and propose a role for circulating dopamine in post-ischaemic vasodilatation äs an explanation for the particular behaviour of dopamine.