URINARY SODIUM AND DOPAMINE EXCRETION .2. ROLE OF HYPERINSUMLINAEMIA IN RENAL DOPAMINE PRODUCTION

Impairment of renal dopamine production could interfere with the sodiu m retention of diabetic patients. In NIDDM patients, glucosuria, induc ed by an OGTT, was accompanied by a paradoxical decline in urinary dop amine (UDA) excretion, which was attributed to the rise in insulinaemi a. The aim of this study was to evaluate the influence of hyperinsulin aemia on renal dopamine production in control subjects. Raising the gl ycaemia within physiological ranges by an invert sugar infusion result ed in a decline in urinary sodium (UNa) and UDA excretion. Overt hyper glycaemia with glucosuria, induced by a dextrose infusion, caused a tr ansient increase of UNa and UDA excretion followed by a decline in bot h parameters. The increases in insulinaemia correlated negatively with the decrease in UDA, suggesting an inhibitory effect of insulin on re nal dopamine production. This negative influence of hyperinsulinaemia could lie at the origin of lower UDA excretion observed in diabetes.