An Acute Infusion of Lactic Acid Lowers the Concentration of Potassium in Arterial Plasma by Inducing a Shift of Potassium into Cells of the Liver in Fed Rats

Abstract

Background: Potassium (K⁺) input occurs after meals or during ischemic exercise and is accompanied by a high concentration of L-lactate in plasma (P_L-lactate). Methods: We examined whether infusing 100 µmol L-lactic acid/min for 15 min would lead to a fall in the arterial plasma K⁺ concentration (P_K). We also aimed to evaluate the mechanisms involved in normal rats compared with rats with acute hyperkalemia caused by a shift of K⁺ from cells or a positive K⁺ balance. Results: There was a significant fall in P_K in normal rats (0.25 mM) and a larger fall in P_K in both models of acute hyperkalemia (0.6 mM) when the P_L-lactate rose. The arterial P_K increased by 0.8 mM (p < 0.05) 7 min after stopping this infusion despite a 2-fold rise in the concentration of insulin in arterial plasma (P_Insulin). There was a significant uptake of K⁺ by the liver, but not by skeletal muscle. In rats pretreated with somatostatin, P_Insulin was low and infusing L-lactic acid failed to lower the P_K. Conclusions: A rise in the P_L-lactate in portal venous blood led to a fall in the P_K and insulin was permissive. Absorption of glucose by the Na⁺-linked glucose transporter permits enterocytes to produce enough ADP to augment aerobic glycolysis, raising the P_L-lactate in the portal vein to prevent postprandial hyperkalemia.