Simultaneous measurement of 5-hydroxytryptophan and l-dihydroxyphenylalanine by high-performance liquid chromatography with electrochemical detection

Shum, Andrew Yau‐Chik; Sole, Michael J.; Loon, Glen R. Van

doi:10.1016/s0378-4347(00)80425-9

Cited by 54 publications

(28 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…None of these methods actually measures norepinephrine synthesis rate, and they each provide different absolute levels for norepinephrine turnover; however, they give comparable indices of changes in catecholamine turnover. 21 -33 -M In contrast to measurement of norepinephrine turnover, tissue catecholamine content does not reflect neuronal activity to that tissue, and, consistent with previous reports, the present study confirms that tissue catecholamine content does not necessarily reflect turnover rate. In rats fed a normal NaCl diet, norepinephrine turnover rate was greater in DS than in DR interscapular brown fat, whereas the converse was true in heart tissue.…”

Section: Discussionsupporting

confidence: 89%

“…21 -32 - 33 Various techniques have been proposed to quantitate norepinephrine turnover in tissues based on the accumulation of L-dopa after inhibition of aromatic L-amino-acid decarboxylase, 21 the decline of [ 3 H]norepinephrine after its intravenous injection, or the measurement of the rate of decline of norepinephrine content after tyrosine hydroxylase inhibition, 20 -M which was the approach used in the present study. None of these methods actually measures norepinephrine synthesis rate, and they each provide different absolute levels for norepinephrine turnover; however, they give comparable indices of changes in catecholamine turnover.…”

Section: Discussionmentioning

confidence: 99%

“…Tissue norepinephrine concentration was measured after separation on a high performance liquid chromatographic reverse-phase column (Ultrasphere; octadecylsilane, 4.6 mm; inside diameter, 25 cm; Altex, Berkeley, CA, USA) by electrochemical detection. 21 Typically, 25 to 100-/xl aliquots of samples were analyzed. Norepinephrine turnover was evaluated by linear regression analysis of the decline of the log norepinephrine tissue concentration over time after tyrosine hydroxylase inhibition.…”

Section: Methodsmentioning

confidence: 99%

“…Norepinephrine turnover was evaluated by linear regression analysis of the decline of the log norepinephrine tissue concentration over time after tyrosine hydroxylase inhibition. 21 The rate constant of amine loss {kj was taken as the slope of log norepinephrine concentration versus time multiplied by 1/0.434.…”

Section: Methodsmentioning

confidence: 99%

See 3 more Smart Citations

Failure of salt loading to inhibit tissue norepinephrine turnover in prehypertensive Dahl salt-sensitive rats.

et al. 1988

View full text Add to dashboard Cite

SUMMARY To determine if alterations of electrolyte balance or sympathetic nervous system activity are present in Dahl salt-sensitive rats (DS) before the onset of hypertension, we compared electrolyte balances, extracellular fluid volume (inulin space), plasma volume (radiolabeled albumin), and norepinephrine turnover in peripheral tissues (heart and interscapular brown fat) in prehypertensive DS and Dahl salt-resistant rats (DR). Animals were maintained for 5 to 7 days on either a "normal" or high NaCl diet. Tissue norepinephrine turnover was evaluated by measuring the rate at whkh norepinephrine content decreased following tyrosine hydroxylase inhibition with a-methyl-p-tvrosine. Blood pressure was higher (p < 0.05) hi DS (135 ± 2 [SE] mm Hg) than hi DR (129 ± 2 mm Hg) and was not affected by the diets. Extracellular fluid volume and net Na + and Cl~ balances did not differ between DS and DR. However, plasma volume was greater hi DS than in DR (p < 0.05). In both fat and heart, norepinephrine turnover was decreased by dietary NaCl loading hi DR (p < 0.01), but not hi DS. Thus, the tendency of the DS to become hypertensive with high NaCl intake may be related to the combined effects of an increased plasma volume and the failure of high dietary NaCl to inhibit peripheral sympathetic nervous system activity. 1 -2 The blood pressure of the Dahl saltsensitive rat (DS) rises with increased NaCl intake, whereas that of the Dahl salt-resistant rat (DR) does not. DS excrete sodium less efficiently than do DR according to some 3 but not all 4 investigators, and evidence for an expansion of the extracellular fluid volume in the pathogenesis of hypertension in this salt-sensitive model is conflicting. 5 ' 6 Alternatively, there is increasing evidence for the participation of the nervous system in the pathogenesis of salt-sensitive hypertension. Lesions of the paraventricular nuclei or the anteroventral third ventricle region protect against the development of hypertension in the DS and other models of saltsensitive hypertension 7 -8 ; chemical sympathectomy with guanethidine or 6-hydroxydopamine also prevents hypertension in DS fed a high NaCl diet.9 -10

show abstract

Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Failure of salt loading to inhibit tissue norepinephrine turnover in prehypertensive Dahl salt-sensitive rats.

et al. 1988

View full text Add to dashboard Cite

show abstract

“…After acid extraction, centrifugation, and filtration, the tissue levels of the precursor DOPA, DA, NE, E, and the metabolite DOPAC as well as the precursor 5-HTP, 5-HT, and the metabolite 5-HIAA were determined by HPLC with electrochemical detection. The HPLC-electrochemical methods were adapted from procedures previously described (26)(27)(28). Plasma CA were analyzed by HPLC as previously described (29).…”

Section: Methodsmentioning

confidence: 99%

Cerebral and Adrenal Monoamine Metabolism in the Growth-Retarded Rat Fetus under Normoxia and Hypoxia

Thordstein

Hedner

1992

Pediatr Res

View full text Add to dashboard Cite

ABSTRACT. The effect of intrauterine growth retardation (IUGR) on cerebral and adrenal monoamine metabolism was studied in the fetuses of eight nulliparous rat dams after unilateral uterine artery ligation on d 18 of gestation.On d 22 (term = 23 d), four dams were subjected to normoxia and four to hypoxia (10% 0 2 ) for 58 min while their hemodynamics and blood gases were monitored. An inhibitor of L-aromatic-decarboxylase (3-hydroxybensylhydrazine) was infused to measure monoamine synthesis rate. After decapitation of the dam, fetuses were delivered by sectio, decapitated, and dissected at -5OC. The body, liver, forebrain, brainstem, and adrenal glands were weighed, and concentrations of monoamine precursors, transmitters, and metabolites were assessed in the three latter organs. The weights of liver and forebrain were reduced in fetuses with IUGR, whereas brainstem and adrenal weights were unaltered. Epinephrine content in adrenals was reduced in proportion to body weight under normoxia but failed to increase under hypoxia as it did in appropriately grown fetuses. There were only minor changes in monoamine metabolism in the brainstem. In the forebrain, however, marked changes were seen, mainly in serotonin metabolism: under normoxia, fetuses with IUGR had decreased levels of serotonin and its metabolite 5-hydroxyindole acetic acid. Under hypoxia, appropriately grown fetuses reduced their concentrations of these substances, whereas fetuses with IUGR paradoxically increased their synthetic activity. It is concluded that a disturbance of central nervous serotonin metabolism prevails in growth-retarded rat fetuses in late gestation and that this disturbance depends on the degree of growth retardation and the degree of perinatal stress. Fetuses and neonates who are small for gestational age because of IUGR are at increased risk to develop both minor (1, 2) and major (3, 4) neurodevelopmental sequelae. This could be due to an increased risk of asphyxia (5) or an increased sensitivity of the CNS in growth-retarded individuals (6). Indications of an altered central nervous function have been found in growthretarded human fetuses [motor function (7,8) and cardiovascular regulation (9)] and neonates [evoked potentials (lo)]. In growthretarded compared to AGA animal fetuses, changes of cerebral circulation (1 1) and evoked potentials (12) have been shown. Moreover, modifications of evoked potentials (6) and MA metabolism (13) are present in newborn growth-retarded animals when compared with AGA animals.Besides their role as neurotransmitters, MA have trophic effects on cerebral development (14), and manipulations of these systems perinatally have longstanding effects on cerebral function (15) and behavior (16,17). These transmitters, i.e. DA, NE, and 5-HT, have also been implied in the pathophysiology of brain damage from various kinds of stress (18)(19)(20). The growth-retarded fetus often suffers from a mild hypoxia (21) and an insufficient supply of essential amino acids (22), which could influence the synthesis of th...

show abstract

Biomedical Uses of High‐Performance Liquid Chromatography with Electrochemical Detection

Mefford¹

1985

Methods of Biochemical Analysis

View full text Add to dashboard Cite

Simultaneous measurement of 5-hydroxytryptophan and l-dihydroxyphenylalanine by high-performance liquid chromatography with electrochemical detection

Cited by 54 publications

References 14 publications

Failure of salt loading to inhibit tissue norepinephrine turnover in prehypertensive Dahl salt-sensitive rats.

Failure of salt loading to inhibit tissue norepinephrine turnover in prehypertensive Dahl salt-sensitive rats.

Cerebral and Adrenal Monoamine Metabolism in the Growth-Retarded Rat Fetus under Normoxia and Hypoxia

Biomedical Uses of High‐Performance Liquid Chromatography with Electrochemical Detection

Contact Info

Product

Resources

About