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PubMed1982

Benserazide and nomifensine in the diagnosis of prolactin-secreting pituitary adenomas.

Benserazide, an inhibitor of dopa-decarboxylase, stimulates prolactin (Prl) release in normal women and in puerperae; nomifensine, a dopaminergic drug able to release dopamine and to inhibit its re-uptake at the post-synaptic level, inhibits Prl release in the same subjects. Similar modifications of Prl release are evident in selected cases of non-tumoral hyperprolactinaemia, while neither drug modifies Prl release in patients with a Prl-secreting pituitary adenoma, in patients with 'functional' hyperprolactinaemia and in patients with 'functional' hyperprolactinaemia and in patients with minor abnormalities of sellar tomography. Neither drug modified Prl release in patients with macro- or microadenomas; several patients in the remaining groups failed to respond to one or both tests, the concordance between the two tests averaging 75%. Patients responding to both tests, to one test or to neither test showed progressively higher basal Prl levels. Since benserazide and nomifensine can indicate the presence of a pituitary adenoma earlier than sellar tomography, our results indicate that patients with no Prl response to one or to both tests probably harbour a pituitary adenoma which cannot yet be revealed by sellar tomography.

Adenoma↗
PubMedDate not supplied

Levodopa pharmacokinetics. Alterations after benserazide, a decarboxylase inhibitor.

Plasma levodopa decay curves appeared to be triexponential up to 6 hr after single intravenous injections of levodopa in rats, rabbits, and dogs. After pretreatment of each of these three species with benserazide (Ro-4-4602), a decarboxylase inhibitor, plasma levodopa concentrations declined biexponentially. Administration of benserazide decreased both total plasma clearance and apparent volume of distribution of levodopa, but did not change the rate constant of the terminal phase of the plasma levodopa decay curve. Thus, decarboxylase inhibition failed to alter the plasma half-life of levodopa.

Animals↗
PubMed1979

Benserazide induces migraine attacks. Irrelevance of concomitant hyperprolactinemia.

Migrainous women underwent acute administration of sulpiride (25 mg i.v.) and benserazide (125 mg per os), both drugs increasing prolactin secretion. A similar increase in prolactin levels was found following the administration of the two drugs. A typical migraine attack was observed only in the 4 women given benserazide. These data, though being preliminary, stress the scarce or irrelevant role of prolactin in the pathogenesis of the migraine attack.

Adult↗
PubMed1991

[A new levodopa benserazide preparation for Parkinson's disease with motor fluctuations refractory to standard L-dopa].

As Parkinson's disease worsens, many patients develop motor fluctuations which usually correlate directly or indirectly with L-dopa plasma levels. A new L-dopa-benserazide HBS preparation (Madopar) a control release pharmaceutical formulation which is activated when it contacts gastric fluid thus providing more stable L-dopa plasma levels, was assayed. Ten patients with a diagnosis of idiopathic Parkinson's disease and motor fluctuations otherwise unresponsive to conventional therapy were selected. The average age was 62 years and the duration of the disease 9 years. The motor status was evaluated on an hourly basis with the King's College Parkinson's disease rating scale; in addition, a nocturnal disability scale (Lees) was used. Out of the 10 patients, 2 dropped out within the first month due to worsening of parkinsonian signs, while 7 of the remainders preferred HBS preparation to the previous treatment. The number of off hours in this group was reduced by 58% and motor fluctuation became less severe. In only 3 cases was it possible to use HBS as monotherapy while in the rest standard L-dopa had to be added, specially as morning doses. The average L-dopa daily dose was increased by 36%. Unwanted effects included psychiatric disturbances in two (in one L-dopa dose had to be reduced) and epigastralgia in one. Our findings suggest that this L-dopa-benserazide control release may be considered an able therapeutic formulation in the control of motor fluctuations in Parkinson's disease.

Adult↗
PubMed1985

Difference spectrophotometric assay of 1,2-diphenolic drugs in pharmaceutical formulations -III. The simultaneous assay of levodopa and benserazide.

A simultaneous assay of levodopa and benserazide in combined formulations is described that utilizes the different spectral properties of the drugs in the presence of germanium dioxide. Difference absorbances are measured at 238 and 292.5 nm between pH 6 solutions of the drugs complexed with germanium dioxide relative to equimolar solutions of the uncomplexed drugs. The concentrations are calculated using two simultaneous equations derived from the difference absorptivities of the individual drugs at 238 and 292.5 nm. The choice of wavelengths for maximum accuracy and precision is discussed. Good recoveries of the drugs in standard mixtures were obtained and satisfactory precision was demonstrated by the relative standard deviations of 0.46% and 1.07% for levodopa and benserazide, respectively, obtained in the replicate analyses of a sample of Madopar capsules. The accuracy of the procedure and the absence of interference from excipients were confirmed by the good agreement in the results for the assay of several batches of Madopar capsules and one of Madopar tablets with those obtained by the manufacturer by an HPLC procedure.

Journal Article↗
PubMed1994

Renal response to amino acid infusion in rats: effect of dopamine receptor antagonists and benserazide.

Previously, we have found that feeding is a dominant factor controlling urinary dopamine excretion (UDA) in conscious rats (Mühlbauer and Osswald 1992). Since the renal response to feeding is also characterized by an increase in glomerular filtration rate (GFR), we wanted to investigate in a first step whether the feeding-induced elevations of GFR and UDA could be causally related phenomena. Therefore, we studied the influence of dopamine synthesis and dopamine receptor blockade on the renal response to amino acid infusion (AA) in thiopental anesthetized rats. AA infusion (n = 7) increased GFR by 33 +/- 7% (P < 0.001) and UDA by 87 +/- 19% (P < 0.001). In the presence of benserazide (BZD, n = 5), an inhibitor of dopamine synthesis, infused i.v. at a dose of 30 micrograms/min/kg, UDA was suppressed to values below detection limit and the AA-induced GFR increase was abolished. Continuous intravenous infusion of the DA1 receptor antagonist SCH 23390 (SCH, n = 7) in a dose of 4.0 micrograms/kg/min did not prevent the AA-induced increase in GFR (33 +/- 3%, P < 0.001) and UDA (97 +/- 12%, P < 0.001). In contrast, S-sulpiride (SUL), a specific DA2 receptor antagonist, infused continuously i.v. in a dose of 5 micrograms/kg/min, completely abolished the AA-induced GFR increase, while UDA was increased 1.6-fold (P < 0.01). Like BZD, both dopamine receptor antagonists did not affect renal sodium excretion substantially. Our results suggest, that endogenous dopamine could act as a mediator in the renal response to amino acid infusion in the rat, most likely by activation of DA2 receptors.

Amino Acids↗
PubMed1984

Regression of cerebellar syndrome with long-term administration of 5-HTP or the combination 5-HTP-benserazide.

A quantitative evaluation of cerebellar ataxia, with an ataxia score (total, static, kinetic) and the measurement of objective values relating to the major symptoms, was used in 21 patients with hereditary ataxias treated for 12 months with high doses (16 mg/kg/day) of d-l-5-HTP, l-5-HTP or the combination d-l-5-HTP (16 mg/kg/day)--benserazide (6 mg/kg/day). The data obtained from regular examination were processed by computer. The ataxia showed a significant regression at the 12th month, mainly in the static forms and speed of speech. l-5-HTP appeared to be more effective than d-l-5-HTP. Regression of the cerebellar ataxia was also observed in non-degenerative conditions such as multiple sclerosis and surgical lesion of the anterior lobe vermis, showing that 5-HTP was active on the cerebellar syndrome in general. The regression of the cerebellar ataxia was very slow in inherited diseases and continued for 2 or 4 months after the treatment stopped. A serotoninergic cerebellar control of movement is discussed.

5-Hydroxytryptophan↗
PubMed1976

Cardiovascular responses to acute hypoxia in dogs pretreated with benserazide and L-DOPA.

In the control dogs, hypoxia induced different hemodynamic modifications (i.e. an increase of arterial blood pressure, heart rate, cardiac output, regional blood flow) which seem to be related to a release of epinephrine. Pretreatment with benserazide (20 mg/kg i.v.) and L-Dopa (50 mg/kg i.p.) either lessened or completely suppressed any sign of sympathetic stimulation. These results suggest that chemoreceptors are centrally inhibited as had been previously proved for baroreceptors.

Animals↗
PubMed1984

Mechanisms involved in the prolactin-releasing effect of benserazide.

The mechanism(s) underlying the prolactin (PRL)-releasing effect of benserazide (Bz), a peripheral inhibitor of L-aromatic amino-acid decarboxylase, was investigated in the rat. In intact male and female rats, Bz was ineffective to increase significantly plasma PRL at 0.8 mg/kg i.p. but elicited an already maximal effect at 1.6 mg/kg. Bz added to in vitro incubated anterior pituitaries (APs) did not alter PRL secretion at the dose of 3.8 X 10(-6)M but increased PRL release at 10(-4)M. Bz, even at very high doses (up to 10(-3) M), did not displace [3H]spiroperidol binding from AP membrane preparations. In rats having had mechanical ablation of the medio basal hypothalamus (MBH), Bz (15 mg/kg i.p.) induced no rise in plasma PRL and did not counteract the striking inhibitory effect of a dopamine (DA) infusion (5 micrograms/kg per min per 120 min). Administration of Bz (15 mg/kg i.p.) into intact male rats decreased significantly the DA concentrations in the median eminence (ME) but not in the residual hypothalamus and the AP. In the same rats 1-dopa (50 mg/kg i.p.) increased significantly the DA concentrations not only in the ME but also in the hypothalamus and the AP. Bz given concurrently with 1-dopa markedly reduced the rise in DA concentrations induced by 1-dopa in the ME, and greatly potentiated the increase in DA concentrations in the hypothalamus. These data indicate that the mechanism whereby a single administration of Bz increases PRL secretion in the rat is not consistent with the postulated DA receptor antagonist action of the drug, but instead implies inhibition of the decarboxylation of 1-dopa at dopaminergic nerve terminals of the ME.

Animals↗
PubMed2004

Simultaneous determination of levodopa and benserazide by stopped-flow injection analysis and three-way multivariate calibration of kinetic-spectrophotometric data.

The simultaneous determination of levodopa and benserazide in pharmaceutical formulations is described, based on the application of multidimensional partial least-squares regression to the kinetic-spectrophotometric data provided by diode-array detection within a stopped-flow injection method where analytes react with periodate. Flow injection parameters were adequately optimized. Accurate analysis is performed with no sample pre-treatment steps, and with minimum experimental effort. Satisfactory recovery results were obtained on a number of synthetic and commercial samples, in the latter case including the comparison with liquid chromatography measurements.

Benserazide↗
PubMed1998

Comparative single- and multiple-dose pharmacokinetics of levodopa and 3-O-methyldopa following a new dual-release and a conventional slow-release formulation of levodopa and benserazide in healthy subjects.

A multiple-dose study was performed to assess the pharmacokinetic profile of a new levodopa/benserazide dual-release formulation (DRF) in comparison with a conventional slow-release formulation (SRF). The study was of an open label, randomized, two-way cross-over design and was conducted in 18 subjects. Assessment of the two formulations was at day 1 (single-dose) and at day 7 after a 5-day t. i.d. pre-treatment (100 mg levodopa and 25 mg benserazide) in fasting state. The pharmacokinetic parameters reflecting bioavailability, accumulation and metabolism of levodopa were determined. The levodopa pharmacokinetics of the new DRF showed rapid absorption (tmax=1.1 h), followed by sustained levodopa plasma concentrations, similar to the SRF. Following multi-dose administration, the peak plasma concentration of the new DRF was 90% higher compared to the SFR (Cmax=2.1 and 1.1 microg/ml, respectively). The bioavailability was significantly increased by 40% (AUC0-infinity=6.1 and 4.3 microg x h/ml, respectively). The new DFR was well tolerated as shown by the low incidence of mild side effects. In conclusion, the results of this study confirmed the levodopa dual-release properties of this new levodopa/benserazide formulation.

Benserazide↗
PubMed1979

Niacin depletion in Parkinsonian patients treated with L-dopa, benserazide and carbidopa.

1. Benserazide and carbidopa, decarboxylase inhibitors used in the treatment of Parkinson's disease, have been shown to inhibit the enzyme kynurenine hydrolase in rat and mouse liver. This results in reduced synthesis of nicotinamide coenzymes from tryptophan, and hence an increased reliance on dietary niacin. 2. Pellagra might be expected as a result of this inhibition of endogenous synthesis of nicotinamide nucleotides, but has not been reported in patients treated with either drug. 3. The urinary excretion of N1-methyl-nicotinamide, a product of nicotinamide nucleotide metabolism, is considerably reduced in patients treated with dopa alone or in combination with an inhibitor of peripheral dopa decarboxylase, to as low as 40% of the control value. This means that many of these patients could be classified as 'at risk' of niacin deficiency, even if not frankly deficient. 4. Patients treated with dopa plus a decarboxylase inhibitor, but not those treated with dopa alone, also show a reduced excretion of xanthurenic acid, and an increased excretion of kynurenine, as would be expected after inhibition of the kynurenine pathway, and possibly indicative of marginal vitamin B6 deficiency.

Adolescent↗
PubMed1995

Acute administration of levodopa-benserazide and tolcapone, a COMT inhibitor, Parkinson's disease.

Tolcapone, a catechol-O-methyltransferase inhibitor, can interfere with the metabolism of levodopa and dopamine and could prolong the motor effect induced by levodopa in parkinsonian patients. To test this hypothesis, we studied the motor effect induced by three acute administrations of a dose of levodopa-benserazide (Madopar) with either 200 mg or 400 mg of tolcapone or placebo, in a double-blind latin-square design. The duration of the on-phase could be compared in 10 parkinsonian patients suffering from square-shaped motor effect. In comparison to placebo, 200 mg and 400 mg of tolcapone significantly increased the mean duration of the on-phase by 61.7 min ( +/- 19.4 SEM) and by 72.2 min ( +/- 18.5), respectively. This clinical effect is suggested to be related mainly to the increase in levodopa area under the curve and half-life induced by tolcapone. The intensity in dyskinesias was increased by 400 mg of tolcapone. Tolcapone appears to be well tolerated and could be helpful as an adjuvant treatment to levodopa in parkinsonian patients with motor fluctuations.

Aged↗
PubMed1988

Bioavailability and acceptability of a dispersible formulation of levodopa-benserazide in parkinsonian patients with and without dysphagia.

The bioavailability of levodopa-benserazide in a standard capsule and a new dispersible tablet was compared in Parkinsonian patients, with (n = 8) and without (n = 8) swallowing difficulties. There was considerable variation within and between subjects, but no significant differences between formulations for any pharmacokinetic parameters, other than an earlier time-peak concentration following the dispersible tablets (P less than 0.01) in non-dysphagic patients. The acceptability of the dispersible tablets in the dysphagic patients was also determined following 7 days regular use. It was felt there were advantages in four of the patients because it was easier to administer or to swallow. The dispersible formulation may offer practical benefits to a minority of Parkinsonian patients without any anticipated loss of therapeutic efficacy.

Aged↗
PubMed1977

Possible mechanism of adverse reaction following levodopa plus benserazide treatment.

1 Rats treated for seven days with seryl-trihydroxybenzylhydrazine (benserazide), and inhibitor of peripheral aromatic L-amino acid decarboxylase (500 mg/kg, daily, i.p.) alone or in combination with L-DOPA methylester (500 mg/kg, daily, i.p.) for seven days showed a moderate but significant decrease of liver aldehyde dehydrogenase (ALDH), without accompanying change in alcohol dehydrogenase (ADH) activity, compared with saline-treated controls. 2 Administration of L-DOPA methylester (500 mg/kg, daily, i.p.) alone for seven days had little effect on liver ADH or ALDH. 3. The combined treatment might be conducive to the in vivo formation of L-DOPA-derived tetrahydroisoquinoline derivatives which might be implicated in L-DOPA produced adverse effects.

Alcohol Oxidoreductases↗
PubMed1981

Differential effect of benserazide (Ro4-4602) on the concentration of indoleamines in rat pineal and hypothalamus.

1 Low doses (50 and 80 mg/kg) of benserazide (Ro4-4602), an aromatic amino acid decarboxylase inhibitor, markedly reduced 5-hydroxytryptamine and melatonin in the rat pineal gland without affecting hypothalamic 5-hydroxytryptamine. 2 This differential effect shows that inhibition of the pineal gland decarboxylase activity is possible, and confirms that the rat pineal gland is accessible to peripherally acting agents.

Animals↗
PubMed1977

Bromocriptine alone or associated with L-dopa plus benserazide in Parkinson's disease.

Twenty-six patients affected by Parkinson's disease were treated with a 2-Br-alpha-ergocriptine (CB 154): 14 cases were given CB 154 alone, and 12 were given CB 154 along with L-dopa plus benserazide (Madopar). Both CB 154 and combined therapy (CB 154+Madopar) induced a significant improvement in total disability score, tremor, rigidity, akinesia, self-sufficiency, and some motor performance tests (dynamic tests). No significant difference was found between results obtained with CB 154 therapy and with Madopar treatment, while the improvement induced by combined therapy (CB 154+Madopar) was significantly higher than that obtained by Madopar alone. The averse reactions caused by CB 154 alone or associated with Madopar are similar to those observed during other dopaminergic treatment. CB 154 alone or combined with Madopar appears to be a useful advance in the management of Parkinson's disease.

Aged↗