1. Intraventricular clonidine and BAY 1470, administered in small doses to conscious renal hypertensive cats, produced a fall in mean blood pressure lasting for a period of 3 h. This fall in blood pressure was accompanied by a marked bradycardia.
2. Pretreatment with intraventricular phentolamine (0.3–6 μmol), piperoxan (0.18–0.74 μmol) or tolazoline (0.35–1 μmol) abolished the hypotensive effects of intraventricular clonidine (74 nmol), whereas pretreatment with haloperidol (2.6 μmol/kg, intraperitoneally), or desmethylimipramine (3.3 μmol/kg, intraperitoneally, or 1.7 μmol, intraventricularly) did not modify the cardiovascular responses to clonidine.
3. Emesis was observed 1 min after intraventricular administration of clonidine (18–112 nmol) or BAY 1470 (0.07–0.14 μmol), which always preceded the cardiovascular actions and was still observed after pretreatment with haloperidol, desmethylimipramine, phentolamine, piperoxan or tolazoline.
4. In conscious hypertensive rats clonidine (0.6 μmol/kg, intraperitoneally) produced a marked fall in blood pressure that was antagonized by centrally acting α-adrenoreceptor blocking agents but not modified by pretreatment with either 6-hydroxydopamine (three doses of 1 μmol, intraventricularly) or 5,6-dihydroxytryptamine (0.1 μmol).
5. It is concluded that the anti-hypertensive responses to clonidine are mediated via stimulation of central α-adrenoreceptors and are independent of central dopaminergic receptors, intact central serotonergic neurons and intact adrenergic uptake mechanisms.