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At least 235 records · Page 13Linked to original sources
PubMed1990

DOPA decarboxylase inhibition does not influence the diuretic and natriuretic response to exogenous alpha-atrial natriuretic peptide in man.

The role of dopamine synthesis in the renal actions of human alpha-atrial natriuretic peptide (alpha ANP) was investigated in six dehydrated volunteers using the DOPA decarboxylase inhibitor carbidopa. Each subject received oral placebo or carbidopa (100 mg) followed by an infusion of alpha ANP 10 pmol.kg-1.min-1 for 1 h. The responses to placebo alone and to carbidopa alone were investigated on separate occasions. alpha ANP produced a similar increase in plasma immunoreactive alpha ANP whether placebo or carbidopa pretreatment had been given. Urinary dopamine excretion was increased by alpha ANP. Carbidopa pretreatment substantially attenuated this increase without affecting the natriuretic or water-diuretic response to alpha ANP. Carbidopa also failed to alter the change in filtration fraction produced by alpha ANP. The results suggest that increased synthesis of intrarenal dopamine is not required for the renal effects of alpha ANP in man.

Adult↗
PubMed1975

Urinary excretion of monoamines and their metabolites in patients with Parkinson's disease. Response to long-term treatment with levodopa alone or in combination with a dopa decarboxylase inhibitor and clinical correlations.

Urinary excretion of DA, DOPAC, 3-MT, HVA, NMA, MA, VMA and 5-HIAA were studied in 33 parkinsonian patients treated with 1.5-7.5 g of levodopa daily for up to six months and in 30 patients receiving levodopa (800-1,000 mg) combined with a dopa decarboxylase inhibitor, benserazide (200-250 mg). Basal urinary excretions were within normal limits except for that of 3-MT which was significantly lower in parkinsonian patients as compared to controls. Levodopa induced an increase of about 400 fold in urinary DA; DOPAC was increased about 300 fold, 3-MT only about 70 fold, but HVA about 300 fold. Urinary NMA and MA did not change but VMA was increased significantly. On the other hand, urinary 5-HIAA was significantly decreased. The amounts of excreted DA and its subsequent metabolities were increased with the continuation of treatment, suggesting inductive phenomena in enzyme systems. During combined treatment with levodopa and benserazide urinary DA was increased, but only to about one tenth the extent seen with levodopa alone. The excretion of DOPAC was about one 20th, of 3-MT about one fourth and of HVA one 25th that seen during levodopa treatment. No signs of enzyme induction were seen. NMA was lowered significantly but MA remained unchanged. VMA was increased and significantly more than during therapy with levodopa alone. 5-HIAA was again significantly decreased and the decrease was significantly greater than that seen with levodopa alone. Some statistically significant correlations were seen between the excretions of NMA, MA and VMA and cardiovascular side effects, indicating an affection on the NA-ergic system by levodopa treatment. Significant correlation between 5-HIAA excretion and clinical improvement of tremor during levodopa treatment may suggest that participation of 5-HT in the mechanism of tremor.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1984

Inhibition of pig kidney dopa decarboxylase by coenzyme-5-hydroxytryptophan adducts.

The effect of N-(5'-phosphopyridoxyl)-L-5-hydroxytryptophan, N-(5'-phosphopyridoxyl)-D-5-hydroxytryptophan and N-(5'-phosphopyridoxyl)-5-hydroxytryptamine on the reactivation of apoDopa decarboxylase to holoenzyme has been investigated. The different degree of inhibition exerted by these adducts has been interpreted on the basis of a different orientation of the 2 isomers of 5-HTP at the active of Dopa decarboxylase.

Animals↗
PubMed1989

Inhibition of brain dopa-decarboxylase by RO 4-4602 infused ICV blocks alcohol drinking induced in rats by cyanamide.

Following the stereotaxic implantation of chronic cannulae for intracerebroventricular (ICV) infusion, rats were given an alcohol preference test to establish their preferred concentration in comparison with water. After alcohol was removed, 15 mg/kg cyanamide was then injected subcutaneously for 4 days in order to maximize volitional intake of single solutions of alcohol, which in these animals ranged from 7 to 15%. The L-dopa-decarboxylase inhibitor benserazide (Ro 4-4602) injected subcutaneously twice daily in doses of 50-100 mg/kg failed to alter the rats' alcohol consumption either in terms of g/kg or proportional values. However, when given ICV twice daily in concentrations of 10 ng-2.0 micrograms per 5.0 microliters volume, benserazide attenuated the rats' alcohol drinking significantly. This reduction occurred in a dose-dependent manner in terms of both absolute and proportional intakes of alcohol. Pre-treatment of the animals with 1.0 microgram benserazide given ICV, when alcohol was removed from the test situation, did not abolish the subsequent ingestion of alcohol but its peripheral administration (50 mg/kg) enhanced drinking. These results suggest that the interference with the metabolic pathway of dopamine or serotonin synthesis, possibly through the mechanism of reduced formation of aldehyde adducts in the brain, markedly alters the pattern of voluntary drinking in the rat. Alternatively, benserazide could act by its central inhibition of aldehyde dehydrogenase, which in turn would concomitantly elevate levels of acetaldehyde and thereby reduce alcohol drinking.

Alcohol Drinking↗
PubMed1978

Effects of levodopa alone and in combination with dopa-decarboxylase inhibitors on plasma renin activity in patients with Parkinson's disease.

Plasma renin activity (PRA) of patients with Parkinson's disease was measured in recumbency, upright position, and after frusemide administration. The results show that the renin responses to both stimuli are significantly reduced as compared with those obtained in a group of normal subjects, while recumbent PRA levels of Parkinsonism patients are not significantly lower than those found in recumbent normal subjects. Levodopa treatment, alone or in combination with two different dopa-decarboxylase inhibitors, benserazide and carbidopa, does not modify the renin response to posture or to frusemide. Although the reduced activity of the renin-angiotensin system can play some role in the genesis of orthostatic hypotensive episodes encountered in patients with Parkinsonism, the greater incidence of orthostatis hypotension in patients treated with levodopa seems to be unrelated to any effect of this drug on the renin release.

Adult↗
PubMed2000

Opposite effects of glutamate antagonists and antiparkinsonian drugs on the activities of DOPA decarboxylase and 5-HTP decarboxylase in the rat brain.

This study measured the activities of L-DOPA and 5-HTP decarboxylase (DDC and 5-HTPDC) in the substantia nigra and corpus striatum of reserpine-treated rats. Acute injection of the NMDA receptor antagonists CGP 40116 (5 mg/kg) and HA 966 (5 mg/kg), and to a lesser extent eliprodil (10 mg/kg), greatly elevated DDC in both structures, whilst having no effect on (nigra) or inhibiting (striatum) 5-HTPDC. L-DOPA (25 mg/kg) on its own inhibited both enzymes in either brain region. The weak NMDA receptor-channel blockers (and antiparkinsonian drugs) budipine (10 mg/kg), memantine (40 mg/kg) and amantadine (40 mg/kg) strongly increased DDC, whilst not affecting or decreasing 5-HTPDC activity in nigra and striatum. The L-DOPA-induced suppression of DDC was mostly reversed by all three antiparkinsonian drugs, whilst L-DOPA-induced inhibition of 5-HTPDC was only reversed by CGP 40116 (striatum only). It is concluded that glutamate exerts a differential physiological influence on the biosynthesis of dopamine and 5-HT in the brain, by tonically suppressing DDC and tonically stimulating 5-HTPDC. The L-DOPA-induced reduction in DDC may help to explain the eventual loss of efficacy of L-DOPA therapy in parkinsonian patients. It is suggested, however, that it may be possible to extend the lifetime of L-DOPA therapy with drugs which potentiate the activity of DDC, such as budipine and the 1-aminoadamantanes.

Animals↗
PubMed1982

Kinetic analysis of stimulation-evoked overflow of noradrenaline and dopamine beta-hydroxylase from the isolated rabbit heart. The effect of DOPA decarboxylase inhibition.

Rabbit isolated hearts were perfused according to a modified Langendorff procedure. Noradrenaline was measured in the venous effluents whereas dopamine beta-hydroxylase was determined in the transmyocardial fluid drained from the interstitium. Calcium-dependent release of noradrenaline and dopamine beta-hydroxylase was evoked by electrical stimulation of the heart for 6 periods of 1 min duration at 30 min intervals. Tetraethylammonium was added to enhance release. As a result of repeated stimulation, the dopamine beta-hydroxylase overflow from the heart declined monoexponentially, whereas the decline of noradrenaline was biexponential. The two phases of decline were unaltered by cocaine, an inhibitor of noradrenaline uptake. However, pretreatment of the rabbits with monofluoromethyldopa, an irreversible inhibitor of DOPA decarboxylase, transformed the biexponential decline of noradrenaline overflow into a monoexponential one with the same rate constant as that of dopamine beta-hydroxylase overflow. The sum of noradrenaline released plus that remaining in the heart was perfectly matched by the area under the curve of noradrenaline overflow values. Using the dopamine beta-hydroxylase overflow curve, the pool size of the soluble enzyme was calculated which, conversely, agreed with the enzyme contained in the 100,000 g supernatant of strongly homogenized unstimulated hearts. Before stimulation, 18% of the total dopamine beta-hydroxylase activity was in the soluble form. Stimulation depleted the hearts of noradrenaline and soluble dopamine beta-hydroxylase in a stoichiometric manner, provided that noradrenaline synthesis was blocked. The present work utilizes a novel method of measuring soluble dopamine beta-hydroxylase that is available for exocytotic release. Under the conditions of repeated stimulation and prolonged action potentials, the only factor interfering with the stoichiometry of noradrenaline and dopamine beta-hydroxylase release is the re-synthesis of noradrenaline.

Animals↗