Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “DOPA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 973 records · Page 54Linked to original sources
PubMed1976

The effect of L-dopa and chlorpromazine on prolactin and growth hormone secretion in normal women.

The time course of simultaneous changes in prolactin (PRL) and growth hormone secretion in response to a single dose of L-dopa and chlorpromazine was determined in normal women. L-Dopa induced greater, but shorter (30 minutes), growth hormone release than concomitant suppression of PRL secretion. The PRL peak following chlorpromazine occurred at the same time as the nadir of PRL after L-dopa (3.5 hours). The quantity of PRL release inhibited by L-dopa equaled the amount of PRL secretion during the period of rebound, suggesting L-dopa inhibits PRL release, but not synthesis, by the pituitary.

Adult↗
PubMed1981

Decrease of vascular angiotensin sensitivity by L-dopa during human pregnancy.

In 27 pregnant subjects (21 treated women and six control subjects), the effect of L-dopa (500 to 1,000 mg orally) on vascular sensitivity to angiotensin II amide (Hypertensin, Ciba) was examined in 16 of these women, 1,000 mg of L-dopa resulted in a significant decrease in vascular responsiveness to angiotensin, i.e., an increase in angiotensin pressor dose from 16.9 +/- 5.0 to 19.6 +/- 4.5 ng . kg-1 . min-1 (mean +/- SD). In women with an initially low angiotensin pressor dose, the changes were more pronounced. In six control subjects, in whom two angiotensin infusion tests were performed consecutively without additional administration of L-dopa, an increase in vasopressor response to angiotensin was demonstrated. Possible causes for the L-dopa-induced decrease in angiotensin sensitivity are discussed: an inhibition of sympathetic nervous activity, a directly lowered total peripheral resistance, a natriuresis and diuresis, and an altered dopaminergic activity in the hypothalamus. It is hypothesized that long-term treatment with L-dopa or bromocriptine might not only decrease angiotensin sensitivity but also elevated pregnancy-induced hypertension.

Angiotensin Amide↗
PubMed1987

Effects of different monoamine oxidase inhibitors on the metabolism of L-dopa in the rat brain.

The influence of monoamine oxidases A and B on the metabolism of dopamine or the expanded dopamine pool following L-dopa administration remains unclear. This study found that treatment of Sprague-Dawley rats with monoamine oxidase inhibitors strongly affected L-dopa metabolism in the brain, but the influence varied with each individual inhibitor. In animals pretreated with pargyline or clorgyline, L-dopa administration led to huge accumulations of dopamine and significantly raised central norepinephrine concentrations. In contrast, similar L-dopa injections in deprenyl-pretreated rats caused only a moderate rise in dopamine and no change in norepinephrine. There seems to be little relationship between the degree of monoamine oxidase inhibition and the accumulation of catecholamines and their metabolites in the rat brain. The effects of monoamine oxidase inhibitors on dopamine accumulation appeared to occur outside the catecholaminergic neurons since in the animals pretreated with 6-hydroxydopamine, which decreased significantly the content of brain catecholamines, dopamine accumulation following L-dopa administration still remained considerable. On the other hand, the influence of monoamine oxidase inhibitors on brain norepinephrine concentrations seemed to originate in the noradrenergic neurons because norepinephrine increase was greatly reduced in rats treated with 6-hydroxydopamine but was restored when the treatment with 6-hydroxydopamine was accompanied by desimipramine which specifically protects noradrenergic stores.

Animals↗
PubMed1987

Studies on the activity of L-threo-3,4-dihydroxyphenylserine (L-DOPS) as a catecholamine precursor in the brain. Comparison with that of L-dopa.

L-Threo-3,4-dihydroxyphenylserine (L-DOPS) was compared with L-3,4-dihydroxyphenylalanine (L-DOPA) with respect to their activities as central amine precursors. The apparent Km value (the substrate affinity) of L-DOPS for aromatic L-amino acid decarboxylase was nearly equal to that of L-DOPA, whereas the vmax value (the rate of decarboxylation) of L-DOPS was much smaller than that of L-DOPA, the penetration of L-DOPS into the brain through the blood-brain barrier was found to be smaller (about one-fourth) than that of L-DOPA but, for an amine precursor, it was still substantial. Unlike L-DOPA, L-DOPS did not cause a marked accumulation of norepinephrine (NE), the corresponding catecholamine in the brain, but nialamide, a monoamine oxidase inhibitor significantly enhanced the L-DOPS-induced rise of NE. Moreover, the brain concentration of 3-methoxy-4-hydroxy-phenylethyleneglycol (MHPG), the principal end metabolite of NE, was increased markedly by L-DOPS. These results suggest that L-DOPS may act as an NE precursor in the brain and activate NE neurons by increasing the turnover rate of NE.

Animals↗
PubMed1989

Vesicular accumulation of dopamine following L-DOPA administration.

In this study, the accumulations of dopamine (DA) and norepinephrine (NE) were measured in the brain tissues and in the synaptic vesicle fractions prepared from whole brain of control rats and rats injected with L-DOPA. In the normal rat brain, a 3-fold increase in DA following L-DOPA administration was followed by a small, but not significant increase in vesicular DA, indicating a restricted vesicular uptake of exogenous DA. At the same time, NE in the vesicular fraction and in the whole brain tissue did not change, suggesting a possible link between DA vesicular uptake of DA and brain NE. However, in rats pretreated with alpha-methyl-p-tyrosine, which significantly (P less than 0.05) reduced DA and NE levels in brain tissues and in the synaptic vesicles, L-DOPA administration led to a significant increase in vesicular DA (P less than 0.05), suggesting that catecholamine depletion may result in greater vesicular uptake of cytoplasmic DA. The increase in vesicular DA was accompanied by increases in tissue and vesicular NE, underscoring again the existence of a link between vesicular uptake of DA and brain NE following L-DOPA administration. The results also demonstrated a large increase in 3,4-dihydroxyphenylacetic acid (DOPAC) following L-DOPA, in the brain tissues but not in the synaptic vesicle, indicating that monoamine oxidase activity is confined to the cytoplasm.

Animals↗
PubMed1985

Effect of L-DOPA on glucose oxidation and incorporation into glycogen in discrete brain regions of the rat.

Previous reports in which the [14C]deoxyglucose mapping technique was used, have demonstrated that systemic administration of L-DOPA can either increase or decrease glucose utilization in various brain regions. However, in the striatum, which contains a high concentration of dopamine, no conclusive results were found using this technique. In the present study we attempted, by implicating a different technique, to evaluate the effect of L-DOPA on glucose metabolism in the striatum. This approach is based on in vitro measuring of glucose oxidation to CO2 and its incorporation to glycogen. Rats were injected with carbidopa (100 mg/kg) and 1 h later with L-DOPA (50 mg/kg). The rats were sacrificed by decapitation 1 h after L-DOPA injection and the following brain regions were assayed for glucose oxidation to CO2 and its incorporation to glycogen: striatum, hypothalamus, hippocampus and prefrontal cortex. A significant increase of glucose oxidation of 50% was found in the striatum and hippocampus, while no change was demonstrated in the hypothalamus and cortex. The incorporation of glucose to glycogen was markedly reduced in the striatum and hippocampus while no change was found in the hypothalamus or cortex. The present results demonstrate that L-DOPA treatment increases glucose metabolism in specific brain areas. The mechanism involved might be an increase in cellular uptake of glucose and/or activation of enzymes participating in glucose metabolic pathways.

Animals↗
PubMed1990

Dopamine- and dopa-immunoreactive neurons in the cat forebrain with reference to tyrosine hydroxylase-immunohistochemistry.

The distribution of cell bodies containing immunoreactivities to dopamine (DA), L-3,4-dihydroxyphenylalanine (DOPA) and tyrosine hydroxylase (TH) was studied immunohistochemically in the cat forebrain especially in the hypothalamus with or without intraventricular administration of colchicine. In normal cats, DA-immunoreactive (IR) neurons, whose intensity of immunostainings was variable from one to another, were localized exclusively in the hypothalamus and showed a distribution pattern similar to that of TH-IR ones. They were distributed in the posterior, dorsal and periventricular hypothalamic areas. Arcuate cells showed no or very weak DA-immunoreactivity. Weak to intense DOPA-IR cells were distributed in a similar manner to DA-IR ones but were far smaller in number. In colchicine-treated animals, DA- and DOPA-immunoreactivities were enhanced particularly in arcuate and dorsal hypothalamic cells. A cluster composed of small DA- and DOPA-IR cells was identified in the area ventral to the mamillothalamic tract equivalent to rat A13c TH-IR cell group. Colchicine treatment enabled us to visualize a large number of TH-IR perikarya in the medial and lateral preoptic areas, anterior commissure nucleus, basal forebrain, area closely related to the organum vasculosum laminae terminalis, and some in the bed nucleus of the stria terminalis as has been reported in other species. However, virtually none of these cells contained detectable DA- and DOPA-immunoreactivities.

Animals↗
PubMed1996

Effects of bromocriptine and/or L-DOPA on neurons in substantia nigra of MPTP-treated C57BL/6 mice.

The effects of bromocriptine and/or L-DOPA on substantia nigra neurons of MPTP-intoxicated mice were investigated. L-DOPA reduced the number of neurons. Bromocriptine protected the neurons from damage by L-DOPA but had no effect on the neurons damaged by MPTP. The treatment of bromocriptine and L-DOPA protected the neurons compared with single administration of bromocriptine. It seems reasonable to suppose that bromocriptine should be added to L-DOPA in order to protect the neurons in parkinsonism.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1988

A new method for the determination of L-dopa and 3-O-methyldopa in plasma and cerebrospinal fluid using gas chromatography and electron capture negative ion mass spectrometry.

L-3-(3,4-Dihydroxyphenyl)alanine (DOPA) and its 3-O-methyl metabolite (OMD) were measured in plasma and cerebrospinal fluid by a new assay which combines N,O-acetylation of amino acids in aqueous media, preparation of pentafluorobenzyl esters under anhydrous conditions, and analysis by gas chromatography-electron capture negative ion mass spectrometry. The N,O-acetyl, carboxy-PFB derivatives gave abundant carboxylate anions ([M-CH2C6F5]-) which were suitable for sensitive analysis using selected ion monitoring. Plasma and CSF samples were sufficiently purified by a simple organic solvent extraction. Analytical recovery for DOPA was 100.2 +/- 3.7% at the level of 100 nmol/l. Analysis of DOPA in plasma was performed with a relative standard deviation of 5%. The limit of quantitation in plasma and CSF was at the sub-nmol/l level. In healthy adults, DOPA concentration in plasma was 9.0 +/- 2 nmol/l (n = 11) and in CSF 3.5 +/- 0.9 nmol/l (n = 9). The concentration of OMD in plasma was 99.1 nmol/l (pool of 24 samples) and 15.3 nmol/l in CSF (pool of 12 samples). Measurement of 5-[2H]DOPA and 5-[2H]OMD in plasma of a healthy individual who had been orally loaded with 3,5-[2H2]tyrosine (150 mg kg body wt) was possible for several hours after the load.

Acetylation↗
PubMed1977

EEG power spectral changes secondary to L-DOPA treatment in parkinsonian patients: a pilot study.

Clinical EEG evaluation and power spectral analysis were performed on 12 parkinsonian patients before and during L-DOPA treatment. The EEG evaluation did not disclose any significant effects of L-DOPA treatment. Spectral analysis disclosed normal interlobar and interhemispheric power differences and an increase in delta and slow-theta power in the right temporal as compared to the right occipital lobe before L-DOPA treatment was initiated. L-DOPA treatment significantly increased alpha power in both occipital lobes, decreased theta power in the right temporal lobe, accentuated power differences in the theta and alpha bands between temporal and occipital lobes and attenuated beta power differences in those areas. This work is intended as a pilot study in the quantitative EEG evaluation of Parkinson's disease and L-DOPA treatment.

Electroencephalography↗
PubMed1979

gamma-Glutamyl DOPA and gamma-glutamyl dopamine: effect on plasma glucose levels.

gamma-Glutamyl-L-3,4-dihydroxyphenylalanine (gamma-glutamyl DOPA) and gamma-glutamyldopamine (gamma-glutamyl DA) are kidney specific prodrugs. Their effect on plasma glucose levels in the rat was compared to that of L-DOPA and dopamine (DA) after a 30 min intravenous infusion. L-DOPA and DA induced hyperglycemia after 15 min of druginfusion. A more marked and protracted elevation of plasma glucose was observed after infusion of gamma-glutamyl DA. By gamma-glutamyl DOPA had no effect on plasma glucose levels in spite of the high accumulation of DA in the pancreas after this prodrug. Of the various dopamine produrgs studied only gamma-glutamyl DOPA was not hyperglycemic in doses that are known to increase renal plasma flow in the rat. A simplified new procedure for the synthesis of gamma-glutamyl DA is described.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1994

Effect of catechol-O-methyl transferase inhibition on peripheral and central metabolism of 6-[18F]fluoro-L-dopa.

In the presence of carbidopa, L-3,4-dihydroxy-6-[18F]fluorophenylalanine ([18F]fluoro-DOPA) is mainly metabolized by catechol-O-methyl transferase. We studied the effects of entacapone, a peripheral catechol-O-methyl transferase inhibitor, on striatal [18F]fluoro-DOPA uptake in rats. Rats were pretreated with carbidopa, entacapone or both before high specific activity (> 2 Ci/mmol) [18F]fluoro-DOPA administration. Entacapone alone antagonized the appearance of methylated metabolites in plasma, striatum and cerebellum but did not increase striatal [18F]fluoro-DOPA availability. Entacapone added to carbidopa significantly increased the striatum/cerebellum total radioactivity ratio (1.4 versus 1.2 in rats with carbidopa, 1.0 in controls) but significant levels of methylated metabolites were found in the brain. Entacapone added to carbidopa might increase the striatum/cerebellum total radioactivity ratio in humans undergoing [18F]fluoro-DOPA positron emission tomography (PET) studies. However, the appearance of methylated metabolites in the brain could hamper quantification of the PET data.

Animals↗
PubMed1996

Ventral tegmental injection of nicotine induces locomotor activity and L-DOPA release from nucleus accumbens.

Effects of nicotine systemically or locally on locomotor activity and L-3,4-dihydroxyphenylalanine (L-DOPA) release were studied using microdialysis in the nucleus accumbens of freely moving rats. The basal L-DOPA release was Ca2(+)-dependent and tetrodotoxin-sensitive. Systemic nicotine (1 mg/kg s.c.) increased locomotor activity and L-DOPA release preferentially in the nucleus accumbens as compared with the striatum. Injection of nicotine (30 micrograms) into the ventral tegmental area increased locomotor activity and L-DOPA release from the nucleus accumbens. These increases were antagonized by prior injection of mecamylamine into the ventral tegmental area. Nicotine induces locomotor activity and L-DOPA release from the nucleus accumbens via nicotinic receptors in the ventral tegmental area. The release may be relevant to behavioral actions of nicotine.

Animals↗
PubMed1991

Changes in dopamine release in vitro from the corpus striatum of young versus aged rats as a function of infusion modes of L-dopa, potassium, and amphetamine.

In the present experiments we examined the effects of two different modes of infusion (two separate 10 min versus continuous infusions) of a depolarizing concentration of potassium (K+, 30 mM), amphetamine (AMPH, 10 microM), or L-DOPA (5 microM) upon dopamine (DA) release in vitro from superfused corpus striatal (CS) tissue fragments of young (2-4 months) and aged (18-24 months) male rats. The relative changes in DA release to two infusions of K+ and AMPH (R2/R1) were virtually identical for CS from both young and aged rats. In the case of L-DOPA, DA release from CS of young rats was markedly increased in response to the second compared to the first L-DOPA infusion (R2/R1 = 2.48 +/- 0.33, N = 7) and significantly greater than that of aged rats (R2/R1 = 1.24 +/- 0.17, N = 6). A continuous infusion of K+ and AMPH resulted in an overall greater amount of DA release from the CS of young versus aged rats. In contrast, DA release from CS of aged rats showed an overall more rapid and greater amount of DA release to continuous L-DOPA infusion than that from the CS of young rats. These results demonstrate age-dependent differences in DA release from the CS as a function of the infusion mode of specific secretagogues. Particularly interesting were the responses to L-DOPA where a pulsatile administration resulted in an overall greater amount of DA release from the CS of young rats while a continuous infusion produced a greater amount of DA release from the CS of aged rats.

Aging↗
PubMed1993

The effect of tryptophan on dopa-oxidation by melanosomal tyrosinase.

1. Tryptophan has been shown to inhibit dopa-oxidation by melanosomal tyrosinase. 2. The inhibition is of mixed-type with Ki = 1.6 x 10(-3) M. 3. Tryptophan does not interact with the oxidation product of the dopa-oxidase reaction. 4. Neither oxygen nor hydroxyl radicals are involved in the inhibition found in presence of tryptophan. 5. Tryptophan, like dopa, also inhibits tyrosine hydroxylase and dopa-oxidase activity of melanosomal tyrosinase and its inhibitory mechanism differs from inhibition due to non-substrate type compounds like cysteine, ascorbic acid. 6. These experiments together with previous findings suggest that the status of tryptophan may be similar to that of dopa in relation to regulation of melanogenesis.

Animals↗
PubMed1982

No evidence for a peripheral effect of L-DOPA on plasma prolactin in the rat.

Male and female rats with two permanently indwelling intravenous catheters were infused for 2 hours with ovine prolactin. During equilibrium conditions the effects of intravenously injected L-DOPA and benzerazide (a blocker of dopa-decarboxylase) on steady state levels of ovine prolactin were measured. A dose of 4.5 mg L-DOPA per 100 gr body weight (b.w.) caused a transient increase of plasma ovine prolactin. A dose of 0.3 mg L-DOPA/100 gr b.w. had no effect, neither in males nor in females, while benzerazide (20 mg/100 gr b.w.) had only a slight effect. The experiments suggest that L-DOPA does not affect the peripheral uptake of prolactin from the plasma.

Animals↗
PubMed1985

A method for very rapid determinations of catechols using ion-pairing reverse phase HPLC with electrochemical detection: effects of L-dopa treatment on the catechol content in various rat brain structures.

A simple and rapid method for determination of 12 catechols (9 endogenous and 3 internal standards, i.s.) using ion-pairing reverse phase HPLC with electrochemical detection is presented. This study basically concentrates on the importance of optimizing the mobile phase composition in isocratic systems where ordinary 25 cm X 4.6 mm i.d. columns are used. Mobile phase compositions for three different purposes are reported: 1) separation of 9 endogenous catechols, possibly occurring in the samples, and 3 i.s. in a moderately short retention time (tR) (L-DOPA, DOPEG, alpha-Methyldopa (alpha-MeDOPA, i.s.), Noradrenaline (NA), DOPAC, Adrenaline (A), Dihydroxybensylamine (DHBA, i.s.), Norsalsolinol (NS), Dopamine (DA), Epinine (EPI), Salsolinol (S) and Isoprenaline (ISO, i.s.) within 11 min), 2) ultra rapid separation of detectable endogenous catechols except L-DOPA (NA, DOPAC, A, DHBA (i.s.), NS and DA within 5.2 min and with S within 5.7 min) and 3) moderately fast separation of detectable endogenous catechols (L-DOPA, NA, A, DHBA (i.s.), NS, DOPAC and DA within 7.6 min and with S within 10 min). By balancing the pH, concentration of organic modifier (2-propanol) and pairing ion (1-heptanesulphonic acid) as well as preconditioning new columns with more packing material (Nucleosil 5 micron C18) and to high pressures (5000 psi) for 7 days, very fast separations with good baseline resolution between the peaks are possible. The method was applied on L-DOPA treated rats (100 mg/kg), where the catechol content was analysed in 7 different brain structures during the time course of synthesis and degradation (4 hours) of catechols from L-DOPA.

Animals↗
PubMed1978

Growth hormone response to propranolol and L--dopa in obese subjects.

Oral administration of propranolol and L-dopa produced a marked increase in plasma growth hormone values in 12 obese subjects who had failed to respond to L-dopa alone. GH values after propranolol and L-dopa in obese subjects were not significantly different from those of normal subjects after L-dopa at 60, 90, and 120 min. Association of propranolol and L-dopa appears to be a simple means of investigating GH response in obese subjects.

Adolescent↗