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  • Title: Potassium-induced renal loss of sodium in lithium-treated rats.
    Author: Olesen OV, Thomsen K.
    Journal: Acta Pharmacol Toxicol (Copenh); 1980 Mar; 46(3):178-84. PubMed ID: 6987825.
    Abstract:
    A high intake of potassium prevents lithium-induced renal water and sodium losing conditions. In order to investigate a probable curative effect of potassium against these conditions Wistar rats were given lithium by the food (80 mmol/kg). The animals had access to water and a 0.46 M NaCl solution. The potassium content of the food was 100 mmol/kg during the pretreatment period of about 4 weeks, then 500 mmol of KCl per kg food was added. Potassium administration did not significantly influence the intake of water but led to a temporary rise of the intake of 0.46 M NaCl. The intake rose from 100 mu to 500 mumol/hr/100 g body weight in the course of 2-3 days and then gradually declined during three weeks. The increase of the sodium intake was not superfluous but due to a renal loss of sodium. If the animals were not allowed to replace the lost sodium by drinking more NaCl solution, plasma renin rose, body weight, lithium clearance, and water intake fell. It is concluded that a high potassium intake was unable to cure lithium-induced water and sodium losing conditions in rats. Prolonged lithium administration interferes with the mechanism for selective renal excretion of potassium. A high potassium intake resulted in a temporary renal loss of sodium.
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