In vivo assessment of decarboxylase inhibition or potentiation: urinary dopamine and L-dopa output after L-dopa administration.
In the L-Dopa treated rat, a decreased urinary output of free and conjugated dopamine and an increase in free and conjugated L-Dopa excretion after administration of decarboxylase-inhibiting drugs provide a good in vivo index of Dopa decarboxylase inhibition. With the exception of free dopamine output, which showed an equivocal change, these measurements appear to provide a good yardstick of decarboxylase status in man also. Using this approach, it was not possible to find any evidence of facilitation of decarboxylase action, in L-Dopa-treated parkinsonians given pyridoxine supplements, to account for the ability of this compound to neutralize the beneficial effect of L-Dopa.
D000818:Animals; D065105:Aromatic Amino Acid Decarboxylase Inhibitors; D001545:Benserazide / Q000494:pharmacology; D002230:Carbidopa / Q000627:therapeutic use*; D004298:Dopamine / Q000652:urine*; D004347:Drug Interactions; D006801:Humans; D006834:Hydrazines / Q000627:therapeutic use*; D007980:Levodopa / Q000494:pharmacology / Q000652:urine*; D010300:Parkinson Disease / Q000188:drug therapy* / Q000652:urine; D011736:Pyridoxine / Q000627:therapeutic use; D051381:Rats
D065105:Aromatic Amino Acid Decarboxylase Inhibitors; D006834:Hydrazines; D007980:Levodopa; D001545:Benserazide; D011736:Pyridoxine; D002230:Carbidopa; D004298:Dopamine