title: 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.
authors.affiliation: Division of Nephrology, St. Michael's Hospital, Toronto, Ont., Canada.
authors.forename: S
authors.initials: S
authors.lastname: Cheema-Dhadli
authors.forename: C-K
authors.initials: CK
authors.lastname: Chong
authors.forename: K S
authors.initials: KS
authors.lastname: Kamel
authors.forename: M L
authors.initials: ML
authors.lastname: Halperin
mesh_terms: D000208:Acute Disease; D000818:Animals; D006728:Hormones / Q000008:administration & dosage / Q000494:pharmacology; D006851:Hydrochloric Acid; D006947:Hyperkalemia / Q000097:blood* / Q000139:chemically induced; D007262:Infusions, Intravenous; D007328:Insulin / Q000097:blood; D019344:Lactic Acid / Q000008:administration & dosage / Q000494:pharmacology*; D008099:Liver / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D008954:Models, Biological; D011188:Potassium / Q000097:blood* / Q000378:metabolism; D011189:Potassium Chloride; D051381:Rats; D013004:Somatostatin / Q000008:administration & dosage / Q000494:pharmacology; D013997:Time Factors
chemical_list: D006728:Hormones; D007328:Insulin; D019344:Lactic Acid; D013004:Somatostatin; D011189:Potassium Chloride; D006851:Hydrochloric Acid; D011188:Potassium