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.

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.