Changes in central monoaminergic function during chronic treatment with clonidine in the spontaneously hypertensive rat

Clonidine was administered intravenously via osmotic minipumps at doses of 0.1 and 0.5 mg · kg^?1 · 24 h^?1. Both doses lowered blood pressure to the same degree by the third day of treatment. Only the higher dose significantly lowered heart rate. There was no tolerance to these cardiovascular effects which were maintained up to the seventh day of clonidine infusion. The only clonidine-induced change in central monoaminergic function was an increase in the adrenaline levels in the hindbrain. No other changes in central monoaminergic function in either cortex or hindbrain were detected at the level of the enzymes (tyrosine hydroxylase) of the neurotransmitters (noradrenaline, dopamine) or of the adrenoceptors ([³H]clonidine binding). Our results suggest that clonidine lowers blood pressure via inhibition of release of hindbrain adrenaline.