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Summary ,1. Human blood platelets have been shown to take up dopamine by an energydependent, saturable process that is inhibited by 5-hydroxytryptamine (5-HT), desipramine and other drugs. 2. Platelets from parkinsonian subjects receiving oral L-DOPA also took up dopamine.3. When the responses of normal and parkinsonian platelets were compared, the parkinsonian cells showed the following differences: increased affinity for the dopamine transport process; decreased equilibrium concentrations of dopamine after incubation for 90 min, and greater efflux of dopamine from loaded platelets during a 10 min incubation. 4. There were no differences in the uptake of 5-HT by parkinsonian platelets, but endogenous 5-HT was significantly reduced; ATP was normal. 5. In two out of three samples of platelets from parkinsonian subjects, traces of a dopamine-like substance were detected, but this finding requires confirmation. 6. If the platelet is a valid model for dopaminergic brain neurones, then the results described would suggest that dopamine uptake and storage may be abnormal in brain neurones in Parkinson's disease.

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SYNOPSISCerebrospinal fluid from patients with subarachnoid haemorrhage and cerebral arterial spasm contracted the isolated basilar artery and potentiated contractions produced by 5-hydroxytryptamine, noradrenaline, and six prostaglandins. The unidentified substance in cerebrospinal fluid probably plays a role in the aetiology of cerebral arterial spasm.We have recently described the contractile responses of the isolated human basilar artery to noradrenaline (NA), 5-hydroxytryptamine (5-HT), and contractile substances derived from human blood . The purpose of these experiments was to develop a human cerebral arterial model which could be used as a basis for investigating a possible association between subarachnoid haemorrhage (SAH) and the presence of vasoactive substances in cerebrospinal fluid (CSF) which may be responsible for the prolonged arterial spasm that often accompanies subarachnoid haemorrhage.We