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PubMed1983

Urinary excretion of O-methylated catecholamines, tyramine and phenyl-ethylamine by volunteers treated with tranylcypromine and CGP 11305 A.

To assess the effect of the new, selective, reversible MAO A inhibitor, CGP 11305 A (4-(5-methoxy-7-bromo-benzofuranyl-2-)piperidine HCl), on MAO A and B activity in man, the daily excretion of total normetanephrine (NMN), metanephrine (MN), 3-methoxytyramine (3-MT) and beta-phenylethylamine (PEA) was measured in the urine of healthy volunteers treated with weekly increasing doses from 40 to 150 mg/d. A similar study was carried out with tranylcypromine in weekly increasing doses from 10 to 25 mg/d. Both compounds increased the excretion of NMN; with CGP 11305 A, a plateau was obtained at 50 mg/d, and tranylcypromine 20 mg was more effective than 10 mg, and was also more active than the highest dose of CGP 11305 A. Increases in MN and 3-MT produced by the latter compound were comparable to that in NMN, whereas tranylcypromine had a biphasic effect on MN excretion, and caused only a small increase in 3-MT excretion. CGP 11305 A up to 150 mg/d did not alter total tyramine excretion, whereas tranylcypromine at 20 mg caused a definite increase. Tranylcypromine led to 4-6 fold increases in PEA output at 20 and 25 mg/d, but not at 10 mg. No such effect could be demonstrated for CGP 11305 A up to 150 mg/d. These results suggest that in man MAO A was inhibited by CGP 11305 A in daily dose of 40 mg or more, whereas it did not affect MAO B at up to 150 mg.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

The dispositional kinetics of phencyclidine and its N-ethylamine analogue in rats.

The uptake kinetics of [3H]-labelled phencyclidine (PCP) and N-ethyl-l-phenycyclohexylamine (PCE) in rats, measured in terms of decreases in the blood concentrations of the drugs after i.v. administration of a single 1.09 mumol dose, were not significantly different. Within a week of administration, the rats excreted about 93% of the [3H]-PCP and about 65% of [3H]-PCE via their urine and faeces; their urine contained nore [3H], mainly as metabolites of [3H]-PCP and of [3H]-PCE, than their faeces. Similarly, more [3H] remained in the tissues of rats treated with [3H]-PCE than in the tissues of [3H4-PCP-treated rats. The fact that PCE is metabolized and excreted more slowly than PCP may account for the higher psychotropic effects of PCE.

Animals↗