Hormone and catecholamine responses accompanying the antinatriuresis of glucose ingestion

The purpose of this study was to determine the importance of various neurohormonal systems in mediating the sodium retention associated with glucose ingestion. Eight normotensive men were randomized to receive, after an overnight fast, glucose (1 mg/kg po) in water, and water alone, during two studies seven to ten days apart. Sodium excretion declined 38 +/- 5% from baseline one to two hours after glucose ingestion (P less than .005), but did not change significantly on the control day. Urinary norepinephrine and dopamine did not change during glucose or control studies. Peak serum insulin levels after glucose correlated inversely with the decline in sodium excretion (r = .67, P less than .10). Plasma renin activity (PRA) increased after glucose ingestion (P less than .01), but changes in PRA did not correlate with changes in sodium excretion. We conclude that the antinatriuresis following glucose ingestion does not result from alterations in noradrenergic-dopaminergic activity or changes in the renin-angiotensin-aldosterone axis. Insulin may modulate renal sodium metabolism directly, or through a yet unknown mechanism.