Abstract

The administration of l-arginine hydrochloride has been used for testing pituitary secretion in humans, and as an experimental model for induction of acute pancreatitis in rats and mice. Whereas in the first case, the administration of the amino acid is associated with hiperkalemia, in the model of acute pancreatitis no data are available on possible changes in potassium homeostasis. The present study shows that the acute administration to mice of l-arginine hydrochloride or other cationic amino acids almost duplicate plasma potassium levels. This effect was associated to a marked decrease of tissue potassium in both pancreas and liver. No changes were found in other tissues. These changes cannot be ascribed to the large load of chloride ions, since similar effects were produced when l-ornithine aspartate was administered. The changes in potassium levels were dependent on the dose. The displacement of intracellular potassium from the liver and pancreas to the extracellular compartment appears to be dependent on the entry of the cationic amino acid, since the administration of an equivalent dose of alfa-difluoromethyl ornithine HCl (DFMO), a non physiological analog of l-ornithine, which is poorly taken by the tissues in comparison with the physiological cationic amino acids, did not produce any change in potassium levels in pancreas and liver. The analyses of the expression of cationic amino acid transporters (CAT) suggest that the CAT-2 transporter may be implicated in the potassium/cationic amino acid interchange in liver and pancreas. The possible physiological or pathological relevance of these findings is discussed.

Highlights

  • Potassium is the principal intracellular cation in the body

  • The aim of the present study was to investigate the levels of potassium in plasma and in different organs after administration of l-arginine and other cationic amino acids, at the doses used to induce acute experimental pancreatitis in mice, in order to know which tissue types drive out potassium to the extracellular compartment after administration of the cationic amino acids

  • The results of the present study indicate that the administration of high doses of cationic amino acids to mice produce a marked increase in potassium plasma levels

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Summary

Introduction

Potassium is the principal intracellular cation in the body. Under normal conditions approximately 98 % of total body potassium is present in the intracellular space, while 2 % is in the extracellular fluid (Forbes and Lewis 1956; Pierson et al 1974). Infusion of l-arginine hydrochloride has been used to stimulate growth hormone secretion (Knof et al 1965; Merimee et al 1965, 1967) This test may Cremades et al SpringerPlus (2016) 5:616 be considered nonhazardous when renal function is normal, different reports have revealed that the treatment may induce dangerous increases of serum potassium concentration in uremic and diabetic patients (Hertz and Richardson 1972; Bushinsky and Gennari 1978; Massara et al 1979). Hyperkalemia after cationic amino acid infusion has been observed in patients receiving infusion of l-arginine and l-lysine for renal protection, during peptide radiotherapy of neuroendocrine tumours (Rolleman et al 2003; Barone et al 2004; Giovacchini et al 2011) In all these cases the tissular origin of the elevation of plasma potassium concentration was not analyzed. There is no data available about a possible alteration of body potassium homeostasis produced by this treatment

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