On the Elimination of Centrally Formed 5‐hydroxyindoleacetic Acid by Cerebrospinal Fluid and Urine

Aizenstein, Moacyr Luiz; Korf, Jakob

doi:10.1111/j.1471-4159.1979.tb11050.x

Cited by 46 publications

(18 citation statements)

References 26 publications

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“…[24][25][26] Hence these urinary metabolites were estimated and considered as indirect indices to assess the levels of respective amines. Similarly, cortisol is metabolized as 6-β-OH cortisol and excreted in urine.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of enalapril affecting the renin-angiotensin system in normal and stress-induced rats based on urinary metabolites of amines and cortisol

Kumar¹,

Satyanarayana

Kilari

2012

J Renin Angiotensin Aldosterone Syst

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Introduction:The renin-angiotensin system is distributed centrally as well as peripherally, which works in association with SNS and HPA in stress. Angiotensin is considered one of the principal hormones for bringing out stress-related changes. To find the influence of enalapril on the neuromediator of CNS and periphery, the present work was carried out. The assessment of the transmitter levels was done by estimating major urinary stress metabolites like vanillylmandelic acid, 5-hydroxyindoleacetic acid, 6-β-hydroxycortisol and homovanillic acid in normal and stress-induced conditions and also in the absence and presence of enalapril treatment in rats. Materials and methods: Groups of rats were subjected to a forced swim stress one hour after daily treatment of enalapril. The 24 h urinary excretion of vanillylmandelic acid, 5-hydroxyindoleacetic acid, 6-β-hydroxycortisol and homovanillic acid was determined in all groups under normal and stressed-induced conditions. Results: Daily administration of enalapril at doses of 3, 10 and 30 mg/kg/body weight inhibited the stress-induced urinary biochemical changes. However, treatment with enalapril in normal conditions increased the excretion of all selected metabolites. Conclusion: It can be speculated that enalapril prevented stress-induced increases of adrenergic, serotonergic and cortical mechanisms.

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Section: Discussionmentioning

confidence: 99%

Evaluation of enalapril affecting the renin-angiotensin system in normal and stress-induced rats based on urinary metabolites of amines and cortisol

Kumar¹,

Satyanarayana

Kilari

2012

J Renin Angiotensin Aldosterone Syst

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“…However, in the lumbar-cisternal perfusion brain metabolism contributes to the outflow. For homovanillic acid (HVA) this contribution has been estimated (Aizenstein and Korf, 1978) and such calculation appeared to be valid also for 5-hydroxyindoleacetic acid (5-HIAA) (Aizenstein and Korf, 1979).…”

Section: Discussionmentioning

confidence: 99%

Origin of free 3-methoxy-4-hydroxyphenylethyleneglycol in rat cerebrospinal fluid

Aizenstein

Postema

et al. 1979

J. Neural Transmission

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The origin of free 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG, a major metabolite of norepinephrine) in rat cerebrospinal fluid (CSF) was investigated using brain and spinal cord perfusions with artificial CSF, electrical stimulation of the locus coeruleus (LC) and the technique of retrograde cell labelling with horseradish peroxidase (HRP). The rates of appearance of MHPG into ventricular-cisternal and lumbar-cisternal perfusates were about 12.4 and 19.2 ng/hour respectively. Probenecid (200 mg/kg i.p.) did not alter the MHPG output in either preparation. Intravenous administration of 3 micrograms MHPG did not substantially enhance the outflow of the metabolite in the ventricular-cisternal perfusate, indicating that MHPG found in the perfusate is of central origin. Maximal activation of central norepinephrine (NE)-containing neurons of the LC by electrical stimulation induced a 50% increase of MHPG levels in the ventricular-cisternal perfusate. In addition HRP was found to be retrogradely transported from the lateral ventricle to these LC-neurons. These findings indicate that MHPG in CSF originates, at least in part from NE of nerve terminals adjacent to the cerebral ventricles, which have their origin in the LC. We calculated that the fraction of MHPG formed in the central nervous system, that was released into the CSF was about 34%. It is concluded that MHPG in CSF is a measure for changes in central NE turnover and that a considerable portion is dependent upon the activity of LC neurons.

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“…The value of using urinary 5-HIAA as an indicator of brain serotonin activity is unclear. Estimates of the amount of urinary 5-HIAA that is derived from brain range from 8% [9] to 34% [10]. Some psychiatric investi gators view urinary 5-HIAA as not being of much value because most of it is derived from the periphery.…”

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confidence: 99%

The Association of the Serotonin Metabolite, 5-HIAA, to the Lysosomal Enzyme N Acetyl-β-Glucosaminidase

et al. 1995

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On the Elimination of Centrally Formed 5‐hydroxyindoleacetic Acid by Cerebrospinal Fluid and Urine

Cited by 46 publications

References 26 publications

Evaluation of enalapril affecting the renin-angiotensin system in normal and stress-induced rats based on urinary metabolites of amines and cortisol

Evaluation of enalapril affecting the renin-angiotensin system in normal and stress-induced rats based on urinary metabolites of amines and cortisol

Origin of free 3-methoxy-4-hydroxyphenylethyleneglycol in rat cerebrospinal fluid

The Association of the Serotonin Metabolite, 5-HIAA, to the Lysosomal Enzyme N Acetyl-β-Glucosaminidase

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