Abstract

1 The contribution of various tissues to some of the pools of catecholamine metabolites in urine has been estimated by measuring the excretion of these compounds by rats given DOPA-free diets and intravenous, intraventricular, or intracisternal 6-hydroxydopamine.2 Destruction of peripheral sympathetic neurones by repeated intravenous doses of 6-hydroxydopamine led to a 34% decrease in noradrenaline excretion, and a 38% decrease in 4-hydroxy-3-methoxyphenylglycol sulphate excretion. Depletion of brain noradrenaline (by 67%), after intracisternal 6-hydroxydopamine, was unassociated with changes in the excretion of noradrenaline or of 4-hydroxy-3-methoxyphenylglycol sulphate. This suggests that these compounds in rat urine are derived mainly from peripheral tissues.3 Depletion of brain dopamine (by 80%) by intraventricular 6-hydroxydopamine was associated with a 27% decrease in the excretion of homovanillic acid. Destruction of peripheral sympathetic neurones with intravenous 6-hydroxydopamine led to a 25% decrease in homovanillic acid excretion. The data suggest that the homovanillic acid in rat urine derives partially from brain dopamine and partially from dopamine released from or metabolized within sympathetic neurones.4 Neither depletion of brain dopamine, nor destruction of sympathetic neurones, caused alterations in the excretion of dopamine or dihydroxyphenylacetic acid.

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