The effect of the dopaminergic system on renal and extrarenal potassium metabolism has been poorly characterized. To examine this problem, 2-hour renal clearance studies were performed in 7 healthy men. Each subject served as his own control and participated in three studies. Subjects received (a) a 2-hour potassium chloride (0.75 mEq/kg) intravenous infusion; (b) the same KCl infusion with dopamine (4 μg/kg · min), and (c) the same KCl infusion with the dopaminergic blocker metoclopramide (10 mg i.v. bolus). The rise in plasma potassium during the KCl infusion was significantly lower in the subjects receiving metoclopramide compared to the controls who received KCl alone (0.29 ± 0.07 vs. 0.52 ± 0.06 mEq/l, p<0.005). During the first 2 h after metoclopramide the increase in U(K)V and total potassium excretion was slightly, although not significantly, lower than in the KCl-alone group (154 ± 15 vs. 168 ± 15 mEq/min, NS). Since the increment in plasma K concentration following metoclopramide was less than in the controls despite a slightly reduced rate of KCl excretion, the improvement in potassium tolerance resulted from an enhanced translocation of potassium from the extra- to intracellular compartment (86 ± 2 vs. 77 ± 3%, p<0.01). There were no significant differences in venous pH, serum bicarbonate concentration or plasma insulin as compared to the control group. When KCl was infused alone, the plasma aldosterone concentration rose from 9 ± 1 to 17 ± 3 ng/ml, p<0.01. When KCl was infused with metoclopramide the increase in plasma aldosterone (7 ± 1 to 35 ± 4 ng/ml, p<0.001) was twice as great as observed with KCl alone (p<0.005). During the 1st h following dopamine infusion, the mean rise in plasma potassium concentration (0.26 ± 0.07 vs. 0.45 ± 0.09 mEq/l, NS) was slightly, though not significantly, lower than in the controls. However, over the entire 3-hour study period there was no difference in the mean increment in plasma potassium between the dopamine infused and control groups. The increase in renal potassium excretion following dopamine plus KCl (226 ± 33 μEq/min) was significantly greater than with KCl alone (126 ± 26 μEq/min, p<0.01). 72 ± 6% of the infused potassium load was excreted following dopamine compared to 56 ± 6% in the control study (p<0.02). The percent of the retained potassium load that was translocated into cells was similar in control (75 ± 5%) and dopamine (80 ± 3%) groups. It can be concluded that (1) dopaminergic blockade with metoclopramide enhances extrarenal potassium disposal by augmenting the translocation of potassium from extracellular to intracellular compartments; (2) dopamine infusion fails to alter extrarenal potassium homeostasis; (3) dopamine increases the renal excretion of potassium, and (4) metoclopramide stimulates aldosterone secretion, whereas dopamine has no effect on plasma aldosterone levels.
|Original language||English (US)|
|Number of pages||8|
|Journal||Mineral and Electrolyte Metabolism|
|State||Published - Dec 1 1987|
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism