Background: Potassium (K+) input occurs after meals or during ischemic exercise and is accompanied by a high concentration of L-lactate in plasma (PL-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 (PK). 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 PK in normal rats (0.25 mM) and a larger fall in PK in both models of acute hyperkalemia (0.6 mM) when the PL-lactate rose. The arterial PK 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 (PInsulin). There was a significant uptake of K+ by the liver, but not by skeletal muscle. In rats pretreated with somatostatin, PInsulin was low and infusing L-lactic acid failed to lower the PK. Conclusions: A rise in the PL-lactate in portal venous blood led to a fall in the PK 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 PL-lactate in the portal vein to prevent postprandial hyperkalemia.

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