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1. Blood pressure and heart rate responses to head-up tilt, standing, the Valsalva manoeuvre, sustained handgrip and cutaneous cold were measured in 27 haemodialysis patients (10 of whom had episodes of haemodialysis-induced hypotension) and 15 control subjects to assess autonomic nervous function. Plasma noradrenaline levels were measured at rest and during head-up tilt. 2. Mean resting supine blood pressure, heart rate and plasma noradrenaline levels were higher in haemodialysis patients than in the control subjects. There was no fall in blood pressure during head-up tilt or standing. The ratio of the R--R intervals of the thirtieth and the fifteenth heart beat after standing (30:15) was lower in the patients; this may be related to their higher resting heart rate. Head-up tilt raised plasma noradrenaline levels in both groups. Heart rate responses to the Valsalva manoeuvre were similar in the patients and control subjects. 3. Systolic blood pressure and heart rate responses to sustained handgrip were similar in both groups. Diastolic and mean blood pressure changes, however, were lower in the patients. The blood pressure and heart rate responses to cutaneous cold were similar in the patients and control subjects. 4. We conclude that generalized autonomic nervous dysfunction does not appear to cause haemodialysis-induced hypotension in patients with chronic renal failure on maintenance haemodialysis.

S U MM ARY Twenty-two patients affected by idiopathic Parkinsonism were studied using the oxygen-15 inhalation technique. The production of labelled metabolic water was found to be decreased in the parietal cerebral cortex, indicating an impairment in oxidative metabolism. This metabolic defect was localised mainly to the parietal cortex of the affected hemispheres; in non-affected hemispheres of patients presenting with unilateral Parkinsonism, the uptake was normal. In contrast, regional blood flow was not significantly altered. It is possible that this metabolic impairment is caused by chronic deafferentation.It has been established that Parkinson's disease is caused by biochemical-metabolic changes which result in an impairment of the normal neurotransmitter balance in the basal ganglia, substantia nigra, and other cerebral regions. It seemed appropriate, therefore, to examine, in life, the full extent of the functional defects in regional cerebral metabolic activity. Such an investigation could provide insight into the overall effects on regional cerebral function and may have implications for the early diagnosis of the disease, and for the development and assessment of therapeutic agents. To this end, a recently developed non-invasive technique using inhalation of radioactive oxygen-15 for the assessment of regional oxygen utilisation and blood flow in the human brain (Jones et al., 1976;Lenzi et al., 1978a) was applied to a group of patients with Parkinsonism. The working hypothesis was that the alteration of neurotransmitter metabolism could be reflected by a modification of local oxygen utilisation and blood flow.

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