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