A rapid quantitative method for the estimation of 5-hydroxyindoleacetic acid in human urine

Contractor, S.F.

doi:10.1016/0006-2952(66)90077-3

Cited by 56 publications

(10 citation statements)

References 9 publications

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“…When 5-HT content had been lowered by p-chlorophenylalanine, the tissue from three birds was pooled for each estimation; the 5-HT and 5-HIAA were estimated by the combined methods of Bertler (1961) and Contractor (1966) as described earlier (Ahtee, Sharman & Vogt, 1970).…”

Section: Methodsmentioning

confidence: 99%

Sleep produced by clonidine (2‐(2,6‐dichlorophenylamino)‐2‐imidazoline hydrochloride)

Holman

Shillito

Vogt

1971

British J Pharmacology

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Summary1. The dose of clonidine (given intravenously) required to elicit sleep in the young chick is 1/25th to 1/50th of an equiactive dose of noradrenaline. The approximate ED50 is 0-01 umol/kg. Phentolamine (10-15 mg/kg, but not 5 mg/kg) antagonizes the action of both clonidine and noradrenaline. 2. Intensive treatment with p-chlorophenylalanine (700 mg/kg for 3-4 days) does not prevent the hypnotic effect of clonidine in the chick, although brain 5-HT is reduced to 15% of normal. Neither is natural sleep modified.3. Sleep after clonidine is not affected by methysergide (0 1-1 ,umol/kg, i.m.), but prevented by LSD (0-1-03 Amol/kg). The effect of LSD is interpreted-as a physiological antagonism. 4. Clonidine (50 mg/kg) injected intravenously into adult rats causes sleep which is not abolished by phentolamine (5 mg/kg) or by p-chlorophenylalanine in doses which interfere with natural sleep. 5. When, per kg body weight, the same dose of clonidine is injected into the lateral cerebral ventricle of rats, sleep ensues in more than half the animals, and persistent eating in about a third; only one -of seventeen rats showed no change in behaviour. Eating and sleeping remained unaltered after p-chlorophenylalanine. The actual dose of clonidine injected into the lateral ventricle was 0 037 ,umol, amounting to about 0 15 ptmol/kg or 15 times the dose required intravenously in the chick. Noradrenaline 0S15 ttmol per (intraventricular) injection caused eating but no sleep, whereas higher doses produced ataxia and paresis. 6. The work suggests that clonidine does not elicit sleep by an action requiring the integrity of the 5-HT-containing neurones arising in the raphe nuclei, and that its action is not on tryptamine receptors. In the chick, sleep appears to be produced by a central sympathomimetic effect; it is possible, but not certain, that this also holds for the rat. 7. The intravenous hypnotic dose of clonidine for the cat is about the same as that for the rat, but injection is not accompanied by signs of peripheral sympathetic stimulation.

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Section: Methodsmentioning

confidence: 99%

Sleep produced by clonidine (2‐(2,6‐dichlorophenylamino)‐2‐imidazoline hydrochloride)

Holman

Shillito

Vogt

1971

British J Pharmacology

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“…Berk & Callingham, 1965) are observed after immunosympathectomy. Uptake of radioactive noradrenaline is reduced at many sites but unchanged at others, while an increase of uptake has been reported in the vas deferens (Sjoqvist, Titus, Michaelson, Taylor & Richardson, 1965 ; Iversen, Glowinski & Axelrod, 1965, 1966: Zaimis et al, 1965.…”

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confidence: 96%

“…By the assay procedure of Contractor (1966), 5-HIAA in acidified urine was selectively adsorbed on Sephadex G-10. After interfering fluorophors had been leached out, 5-HIAA was eluted with 0-02N NH,OH.…”

Section: Conijui Ationi Of Vma In Rat Luriniementioning

confidence: 99%

Catecholamine and 5‐hydroxyindole metabolism in immunosympathectomized rats

Ceasar

Ruthven

Sandler

1969

British J Pharmacology

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1. The daily urinary excretion of normetadrenaline, metadrenaline, 4-hydroxy-3-methoxyphenylglycol, 4-hydroxy-3-methoxymandelic acid, dopamine. homovanillic acid, 5-hydroxytryptamine and 5-hydroxyindolylacetic acid has been estimated in the urine of immunosympathectomized and control rats. 2. A method is given which allows separate spectrophotometric determination of 4-hydroxy-3-methoxyphenylglycol and 4-hydroxy-3-methoxymandelic acid in the same sample of rat urine. Metadrenaline and normetadrenaline were estimated by a modification of the method of Anton & Sayre (1966). 3. Approximately 170, of the 4-hydroxy-3-methoxymandelic acid in rat urine is excreted in the free state, over 60',, as a glucuronide conjugate and the remainder as a sulphate conjugate. 4. Urinary excretion of 4-hydroxy-3-methoxyphenylglycol was approximately halved in immunosympathectomized rats (P<0 001). 4-Hydroxy-3-methoxymandelic acid output was significantly increased in treated animals (P<005) when expressed in terms of body weight. No significant difference was detected for any of the other compounds investigated. 5. The results are discussed in the light of previous knowledge of the effect of immunosympathectomy on catecholamine metabolism.

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“…The estimations of 5-HT and 5-hydroxyindole acetic acid (5-HIAA) were made in the same sample by a fluorimetric method combining those of Bertler (1961) and Contractor (1966). Details have been published (Ahtee, Sharman &Vogt, 1970, and.…”

Section: Chemical Estimationsmentioning

confidence: 99%

The effect of lowering the 5‐hydroxytryptamine content of the rat spinal cord on analgesia produced by morphine

Vogt¹

1974

The Journal of Physiology

205

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SUMMARY1. Injection of 5,6-dihydroxytryptamine (5, 50 ,tg) into a lateral cerebral ventricle of male rats lowered the 5-hydroxytryptamine (5-HT) content of the lumbar cord to 12.8% and reduced the analgesic effect of low doses of morphine (0.64-1.63 mg/kg), tested by exerting pressure on the foot; after doses of morphine of 1.33-1-63 mg/kg, the analgesic response was reduced or abolished in 33 % of the rats, and after 0*64 mg/kg, 58 % of the animals failed to respond normally.2. Two days after an i.P. injection of p-chlorophenylalanine (pCPA, 320 mg/kg), the loss of analgesic potency of morphine was more pronounced than after intraventricular 5,6-HDT. The 5-HT content was lowered to about 8% in the lumbar cord, and to 20% or less in pons and medulla.3. The experiments show that interference with the descending tryptaminergic axons innervating the cord is by itself sufficient to reduce analgesia due to morphine, but they do not exclude the possibility that other tryptaminergic neurones take part in the effect of pCPA. The contribution to the analgesic effect of morphine made by the interaction of tryptaminergic axons with the interneurones 'gating' the afferent impulses in the posterior columns is discussed.

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A rapid quantitative method for the estimation of 5-hydroxyindoleacetic acid in human urine

Cited by 56 publications

References 9 publications

Sleep produced by clonidine (2‐(2,6‐dichlorophenylamino)‐2‐imidazoline hydrochloride)

Sleep produced by clonidine (2‐(2,6‐dichlorophenylamino)‐2‐imidazoline hydrochloride)

Catecholamine and 5‐hydroxyindole metabolism in immunosympathectomized rats

The effect of lowering the 5‐hydroxytryptamine content of the rat spinal cord on analgesia produced by morphine

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