The centrally mediated cardiovascular changes induced by clonidine were studied in conscious rats. Clonidine administered intracerebroventricularly (i.c.v.), and intravenously (i.v.) caused hypotension following an initial pressor response. I.v. clonidine caused significant greater hypotension than i.c.v. clonidine (30 micrograms/kg; p less than 0.05). With the 30 micrograms/kg i.c.v. dose, a tachycardia was observed in all rats following initial transient bradycardia. No tachycardia was observed when clonidine was administered i.v. Propranolol (3 mg/kg i.v.) did not modify the cardiovascular actions of i.c.v. clonidine except initial pressure response. While combined treatment with propranolol (3 mg/kg i.v.) and atropine (1 mg/kg i.v.) abolished both the bradycardic and tachycardic actions of i.c.v. clonidine (30 micrograms/kg), but did not modulate the hypotensive action. Yohimbine (30 micrograms/kg i.c.v.) converted the hypotension induced by i.c.v. clonidine (30 micrograms/kg) to hypertension, attenuated the bradycardia but did not modulate the tachycardia. The same dose of i.c.v. yohimbine attenuated the hypotensive effect of i.v. clonidine (30 micrograms/kg) but did not affect the initial pressor response. Prazosin (30 micrograms/kg i.c.v.) did not modulate either phase of the heart rate response to i.c.v. clonidine. These results provide evidence of centrally mediated pressor and tachycardic actions of clonidine in conscious rats. The tachycardia appears to be mediated through the inhibition of parasympathetic tone and is not dependent on alpha-adrenoceptor mechanism. In conscious rats the opposing influence of centrally mediated pressor and depressor actions may result in the apparently low hypotensive potency of i.c.v. clonidine.