Sodium valproate-induced hyperammonemia in the rat: role of the kidney.
The intravenous injection of sodium valproate (VPA) 200 mg/kg provoked in fasting rats a 100% increase in the arterial NH+4 concentration by the 10th min. The increase persisted at this level for at least 100 min. Simultaneous measurements of NH+4 and glutamine concentrations in the carotid artery, renal vein and suprahepatic vein showed that there were increases in the release of NH+4 and the uptake of glutamine by the kidney while the [NH+4] of suprahepatic venous blood remained stable. In binephrectomized rats injected with VPA, NH+4 levels did not change. These results suggest that the VPA-induced arterial hyperammonemia depended on the accelerated catabolism or possibly the reduced synthesis of glutamine by the kidneys. The liver of fasting rats does not seem to play a preponderant role in the VPA-induced hyperammonemia.
D000641:Ammonia / Q000097:blood* / Q000652:urine; D000818:Animals; D005973:Glutamine / Q000652:urine; D007668:Kidney / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D009392:Nephrectomy; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors; D014635:Valproic Acid / Q000494:pharmacology*
D005973:Glutamine; D014635:Valproic Acid; D000641:Ammonia