The effects of intracisternal injection (i.c.i.) of clonidine (1 microgram kg-1) on blood pressure and heart rate were studied in conscious rabbits with an implanted catheter in the cisterna magna. Each animal was studied under control conditions and 7 days after i.c.i. of 6-hydroxydopamine (6-OHDA) (1 microgram kg-1; n = 10) or ascorbic acid vehicle (n = 6). In the control experiments blood pressure and heart rate began to fall 1--2 min after i.c.i. of clonidine, with maximum falls at 10--20 min averaging 18 +/- 2 mmHg and 45 +/- 8 b/min and almost complete recovery by 90 min. After vehicle pretreatment neither response was significantly altered. After 6-OHDA the early component of the bradycardia was abolished and only a late fall in heart rate developed 30 min after i.c.i. clonidine. The magnitude of the hypotension was unaffected but the onset was slightly delayed, probably owing to the abolition of the bradycardia. The dose of 6-OHDA reduced spinal cord catecholamines to about 20% of the level observed after vehicle. Central catecholaminergic pathways are thus important in the early predominantly vagal component of the clonidine induced bradycardia, but play little role in the hypotensive response.