The conversion in vivo of d-amphetamine to (+)-p-hydroxynorephedrine

Goldstein, Menek; Anagnoste, B

doi:10.1016/0304-4165(65)90412-5

Cited by 106 publications

(15 citation statements)

References 3 publications

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“…For example, increasing hydroxylation or alpha-carbon methylation of the phenethylamine backbone produces al terations in hydrophobicity, in affinity for the neuronal uptake and granular uptake carriers and in susceptibility to metabolism by mono amine oxidase and DA-(3-hydroxylase [Pro test and Blaschko, 1959;Cho et al, 1975;Crcxcling ct al., 1962;Carlsson and Waldeck, 1966;Iversen, 1967], The R(-)enantiomer of POHA was selected since it has a low affinity for DA-P-hydroxylase [Goldstein and Anagnoste. 1965], and its actions would reflect only those of POHA and not PHNE.…”

Section: Introductionmentioning

confidence: 99%

Sympathomimetic Amine-Induced Release of Norepinephrine-<sup>3</sup>H from Different Intraneuronal Storage Compartments

Takimoto¹,

Amiri²,

Cho³

1981

Pharmacology

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The effects of different loading procedures on norepinephrine-³H (NE-³H) efflux induced by a structurally analogous group of indirectly acting sympathomimetic amines was examined in rabbit vas deferens. (+)-Amphetamine was ineffective in releasing ³H from tissues with intact intraneuronal storage granules but was an effective depletor of (a) non-granular intraneuronal compartment(s) following in vivo treatment with reserpine. (±)-p-Hy-droxynorephedrine was a less effective depletor of non-granular NE-³H. These experiments provide further evidence in support of multiple intraneuronal storage compartments which can be pharmacologically differentiated by utilizing indirectly acting sympathomimetic amine agents.

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Section: Introductionmentioning

confidence: 99%

Sympathomimetic Amine-Induced Release of Norepinephrine-<sup>3</sup>H from Different Intraneuronal Storage Compartments

Takimoto¹,

Amiri²,

Cho³

1981

Pharmacology

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“…or local injection) with the AMPH doses from other studies using systemic injections, since we did not measure the actual concentration of p-OHA in the regions of interest. Furthermore, AMPH is first metabolized to p-OHA in the periphery and brain, which is then further hydroxylated to p-OHN (Axelod 1970;Goldstein and Contrera 1962;Goldstein and Anagnoste 1965), and p-OHA does not easily cross the blood-brain barrier.…”

Section: Discussionmentioning

confidence: 99%

Central administration of p-hydroxyamphetamine produces a behavioral stimulant effect in rodents: evidence for the involvement of dopaminergic systems

et al. 2009

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“…Amphetamine is primary metabolized by hydroxylation (Axelrod, 1954;Goldstein & Anagnoste, 1965;Williams, 1967); a phenomenon which may competitively inhibit p-hydroxylation of PEA to p-tyramine. Increased PEA excretion following the administration of either PEA or pargyline to man is accompanied by a concomitant increase in p.…”

Section: Discussionmentioning

confidence: 99%

A Study on the Acute Effect of Amphetamine on the Urinary Excretion of Biogenic Amines and Metabolites in Monkeys

Chuang

Karoum

Perlow

1981

British J Pharmacology

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1 The effects of an acute dose (3 mg/kg) of amphetamine on the urinary excretion of phenylethylamine (PEA), p-tyramine, their metabolites, catecholamine metabolites and phydroxymandelic acid, a major metabolite of p-octopamine were evaluated in the monkey. Amphetamine excretion was also measured. 2 Amphetamine was slowly eliminated from the body, being found in the urine at least six days after administration. 3 Amphetamine increased the excretion of PEA and decreased that of its major metabolite, phenylacetic acid (PAA). This pattern of changes is similar to that previously found in the urine of chronic schizophrenics. 4 The excretion of the dopamine metabolite, 3,4-dihydroxphenylacetic acid (DOPAC) was markedly reduced, that of vanilmandelic acid (VMA) remained unchanged while 3-methoxy-4-hydroxyphenylglycol (MHPG) was increased on the day of drug administration and persisted for at least a further six days. A similar extended effect on the excretion of p-hydroxymandelic acid (it was reduced) was also observed. 5 The excretion of p-tyramine but not its metabolite, p-hydroxyphenylacetic acid, was decreased by amphetamine during treatment and returned to normal levels six days later. 6 From the results obtained, it was concluded that amphetamine effects on behaviour cannot exclusively be attributed to its influence on catecholamines and that other biogenic amines may be involved.7 Since PEA elicits many behavioural changes similar to those seen with amphetamine, and since amphetamine increases PEA excretion, we suggest that amphetamine may exert some of its behavioural responses through the release of PEA.

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The conversion in vivo of d-amphetamine to (+)-p-hydroxynorephedrine

Cited by 106 publications

References 3 publications

Sympathomimetic Amine-Induced Release of Norepinephrine-<sup>3</sup>H from Different Intraneuronal Storage Compartments

Sympathomimetic Amine-Induced Release of Norepinephrine-<sup>3</sup>H from Different Intraneuronal Storage Compartments

Central administration of p-hydroxyamphetamine produces a behavioral stimulant effect in rodents: evidence for the involvement of dopaminergic systems

A Study on the Acute Effect of Amphetamine on the Urinary Excretion of Biogenic Amines and Metabolites in Monkeys

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