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To investigate the source and physiological significance of urinary free dopamine (f-DA) in high sodium diet (8% NaCl) loading, the effects of renal denervation and administration of carbidopa, an inhibitor of peripheral dopa decarboxylase, on urinary f-DA excretion were studied in male Wistar rats. Carbidopa was orally administered in a dose of 20mg/kg every 12h. To ascertain the extent of denervation, kidney norepinephrine was measured. Catecholamines were assayed by HPLC with electrochemical detection. Urinary f-DA and sodium excretion were significantly increased in response to the added NaCl. There were few effects of renal denervation on urinary excretion of f-DA and sodium in high sodium diet loading, whereas carbidopa caused a significant fall not only in urinary f-DA excretion but also in urinary sodium excretion. A highly significant correlation was also found between sodium excretion and f-DA excretion on the 5th day of carbidopa treatment. The data indicates that urinary f-DA in a high sodium diet is mainly derived from the renal tubular cells but not from renal nerves and that f-DA may be an important natriuretic hormone.

The Source and Significance of Increased Urinary Dopamine Excretion during Sodium Loading in Rats