EVIDENCES OF A SYMPATHOADRENAL DYSFUNCTION AFTER LESION OF THE CENTRAL NORADRENERGIC PATHWAYS IN RATS
EVIDENCES OF A SYMPATHOADRENAL DYSFUNCTION AFTER LESION OF THE CENTRAL NORADRENERGIC PATHWAYS IN RATS
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DOI：
10.1007/bf01243348
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发表时间：
1986-01-01
影响因子：
3.3
通讯作者：
DAJAS, F
中科院分区：
文献类型：
--
作者：
BARBEITO, L;FERNANDEZ, C;DAJAS, F
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 .mu.g/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.
