Potassium deficiency decreases the capacity for urea synthesis and markedly increases ammonia in rats

Our study provides novel findings of experimental hypokalemia reducing urea cycle functionality and thereby severely increasing plasma ammonia. This is pathophysiologically interesting because ammonia increases during by a hitherto unknown mechanism, which may be particular important in relation to the unexplained link between hepatic encephalopathy. Potassium deficiency decreases gene expression, protein synthesis, growth. The maintains body nitrogen homeostasis including removal toxic Hyperammonemia an obligatory trait liver failure, risk for encephalopathy, reported increase We aimed clarify effects on vivo capacity cycle, genes enzymes involved, concentrations. Female Wistar rats were fed potassium-free diet 13 days. Half then potassium repleted. Both groups compared with pair- free-fed controls. following measured: urea-nitrogen synthesis (CUNS); expression (mRNA) enzymes; potassium, sodium, ammonia; intracellular magnesium liver, kidney, muscle tissues; sodium/potassium pumps. Liver histology was assessed. induced 1.9 ± 0.4 mmol/L. Compared pair-fed controls, CUNS reduced 34% ( P < 0.01), argininosuccinate synthetase 1 ASS1) decreased 33% 0.05), concentrations eightfold elevated 0.001). Kidney tissue contents markedly but unchanged tissue. Protein expressions pumps unchanged. Repletion reverted all changes. Hypokalemia via effects. intervention led marked hyperammonemia, quantitatively explainable compromised cycle. motivate clinical studies patients disease.