Effects of clonidine on the cerebral adrenaline turnover and the adrenaline release in nucleus tractus solitarii of the rat

The dopamine β-hydroxylase inhibitor, FLA 63 reduced the adrenaline levels in the hypothalamus, A₁ and A₂ regions. Clonidine (O.1 to 1 mg/kg, sc.) retarded the FLA63-induced disappearance of adrenaline in all of the areas investigated. This effect of clonidine was antagonized by the simultaneous administration of yohimbine (1 and 10 mg/kg, ip.) or phenoxybenzamine (2O mg/kg, ip.). In addition, yohimbine (10 mg/kg, ip.) administered alone, increased the rate of adrenaline disappearance caused by the inhibition of dopamine-β-hydroxylase. In rat nucleus tractus solitarii slices superfused with Krebs' solution, clonidine (1 μM) decreased the ³H-adrenaline overflow elicited by a 2 min exposure to 3O mM potassium. While the specific presynaptic α-blocking agent, yohimbine (1 μM) increased the potassium-evoked tritium efflux, prazosin (O.3 μM) and WB 4101 (0.3 μM) which block preferentially peripheral α-postsynaptic adrenoceptors were ineffective in this respect. The above results suggest that clonidine decreases adrenaline turnover in the brain through activation of receptors with α2 pharmacological characteristics probably localized on adrenaline terminals.