Evidences of a sympatho-adrenal dysfunction after lesion of the central noradrenergic pathways in rats.

Abstract

The urinary excretion rates of noradrenaline and adrenaline--as an index of sympatho-adrenal activity--were assessed in a group of rats previously treated with the noradrenergic toxic agent DSP-4. The suppressive effects of clonidine (10 micrograms/kg) on urinary NA excretion were also evaluated. Basal noradrenaline and adrenaline excretion rates were higher in DSP-4 treated rats than in controls. Clonidine elicited a marked suppression of urinary noradrenaline excretion rates in control rats but not in those treated with DSP-4 90-120 days before. Endogenous catecholamine level determinations, 120 days after DSP-4 administration, evidenced, on the one hand, an almost complete depletion of noradrenaline levels in spinal cord, cerebral cortex, and hippocampus. On the other hand, a significant increase of noradrenaline in the kidney and of adrenaline in the adrenal gland was found. These results are interpreted as indicating that the lesion of central noradrenergic pathways induces a sympatho-adrenal hyperactivity as well as an impaired response to alpha-2 adrenergic receptor agonists.