Krishna G G, Danovitch G M, Beck F W, Sowers J R
J Lab Clin Med. 1985 Feb;105(2):214-8.
Previous studies have shown a direct relationship between urinary sodium excretion and both urinary dopamine excretion and plasma dopamine levels. The significance of this relationship is unclear. We therefore studied the effect of dopaminergic blockade on the renal response to volume expansion produced by the infusion of 2 L 0.9% saline solution intravenously over 4 hours in a group of six healthy adult volunteers previously shown to have appropriate sodium balance. The dopamine receptor antagonist metoclopramide was administered intravenously at a dose of 10 mg/hr throughout the study period; a separate group of control subjects received saline infusion without metoclopramide. During saline infusion urinary sodium excretion increased steadily in controls, from a basal level of 127 +/- 25 mu Eq/min to a peak value of 451 +/- 83 mu Eq/min (p less than 0.005) during the fourth hour of infusion. The study group receiving saline solution along with metoclopramide failed to show any significant increase in urinary sodium excretion over the basal levels. Cumulative sodium excretion during saline loading was significantly less in those receiving saline solution with metoclopramide (55 +/- 14 mEq) than in controls (101 +/- 15 mEq)(p less than 0.05). The plasma aldosterone levels in the control group receiving saline solution alone fell steadily from a preinfusion level of 11.0 +/- 0.9 ng/dl to the nadir of 6.5 +/- 0.9 ng/dl (p less than 0.02), reached during the third hour of infusion. In contrast, in the study group receiving saline solution with metoclopramide, the plasma aldosterone levels remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)