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EFFECT OF APOMORPHINE ON ADRENAL MEDULLARY CATECHOLAMINE LEVELS

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Summary—The effects of the dopamine receptor agonist, apomorphine, on the total catecholamine content of the adrenal medulla were studied in normotensive rats. Apomorphine (3, 15, 30 mg/kg SC) induced a dose‐dependent decrease in catecholamine content of the adrenal gland. The action of apomorphine was suppressed by previous treatment with the non specific dopamine receptor antagonist, haloperidol (9 mg/kg 1P), or the D2 antagonist domperidone (2 mg/kg 1P), but not by the D1 antagonist SCH 23390 (1 mg/kg 1P). The apomorphine‐induced decrease in adrenal catecholamine concentration was suppressed by denervation of the adrenal medulla,i.e.unilateral section of splanchnic fibers performed 5 days before. These results show that, under our experimental conditions, the effect of apomorphine is due to the activation of D2 dopamine receptors probably located on splanchnic nerve endings and suggest the existence of a peripheral D2 dopaminergic system which modulates adrenal medullary catecholamine content.
Title: EFFECT OF APOMORPHINE ON ADRENAL MEDULLARY CATECHOLAMINE LEVELS
Description:
Summary—The effects of the dopamine receptor agonist, apomorphine, on the total catecholamine content of the adrenal medulla were studied in normotensive rats.
Apomorphine (3, 15, 30 mg/kg SC) induced a dose‐dependent decrease in catecholamine content of the adrenal gland.
The action of apomorphine was suppressed by previous treatment with the non specific dopamine receptor antagonist, haloperidol (9 mg/kg 1P), or the D2 antagonist domperidone (2 mg/kg 1P), but not by the D1 antagonist SCH 23390 (1 mg/kg 1P).
The apomorphine‐induced decrease in adrenal catecholamine concentration was suppressed by denervation of the adrenal medulla,i.
e.
unilateral section of splanchnic fibers performed 5 days before.
These results show that, under our experimental conditions, the effect of apomorphine is due to the activation of D2 dopamine receptors probably located on splanchnic nerve endings and suggest the existence of a peripheral D2 dopaminergic system which modulates adrenal medullary catecholamine content.

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