STIMULATORY EFFECT OF THE DOPA-DECARBOXYLASE INHIBITOR Ro 4-4602 ON PROLACTIN RELEASE; INHIBITION BY L-DOPA, METERGOLINE, METHYSERGIDE AND 2-Br-α-ERGOCRYPTINE

Pontiroli, Antonio E.; Castegnaro, E; Vettaro, M. P.; Viberti, Giancarlo; Pozza, G.

doi:10.1530/acta.0.0840036

Cited by 29 publications

(25 citation statements)

References 19 publications

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“…Our data indicating that benserazide in creases the serum levels of prolactin in man are consistent with those of Pontiroli et al (1977). If the employed dose is considered, a dose dependence of the effect of Ro 4-4602 on serum prolactin levels may be suggested, since, in our hands, the mean peak obtained with the 125-mg dose is considerably higher than that reported by Pontiroli et al for the dose of 50 mg.…”

Section: Discussionsupporting

confidence: 91%

“…Dopamine is, in fact, known to act also directly on the anterior pituitary and inhibit prolactin secretion (MacLeod, 1969). The fact that bromocriptine, a dopaminergic drug acting also at the pituitary level in depressing prolactin secretion (Pasteels et al, 1971), counteracts benserazide effects when administered together to humans (Pontiroli et al, 1977), supports this view.…”

Section: Discussionmentioning

confidence: 99%

“…Pontiroli et al (1977) have shown that the administration of 50 mg of benserazide to humans increases serum prolactin levels. The finding is particularly interesting because it sug gests the possibility of studying the secretion of prolactin and its regulation by altering selective ly monoamine concentrations in the involved structures, both inside and outside the bloodbrain barrier.…”

Section: Introductionmentioning

confidence: 99%

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Lack of Counteracting Effect of Liposomes on Benserazide-Induced Hyperprolactinemia

et al. 1979

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Benserazide induces an increase of serum prolactin in man, possibly as the result of an impairment of the dopamine effect on the pituitary and/or on the outer median eminence caused by the inhibition on L-dopa decarboxylase. On the other hand, liposomes obtained from bovine brain cortex phospholipids reduce serum prolactin possibly through an effect of phosphatidylserine on dopamine biosynthesis at the level of tyrosine hydroxylase. Benserazide, given orally (125 mg) to 5 normal subjects, induced an increase of serum prolactin that did not change when 300 mg of phospholipid liposomes were given intravenously 60 min later. An increase of L-dopa synthesis does not seem to be capable to overcome the effects of the decarboxylase inhibition.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Lack of Counteracting Effect of Liposomes on Benserazide-Induced Hyperprolactinemia

et al. 1979

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“…In the present study the use of peripheral decarboxylase inhibitors in combination with the administration of amino acid precursors was avoided since the rat's blood-brain barri er is still immature during the first postnatal week [25,28] and, in addition, most of these substances are reported to have pronounced behavioral and neuroendocrine effects by themselves [8,26].…”

Section: Discussionmentioning

confidence: 99%

The Role of Dopaminergic and Serotonergic Mechanisms in the Development of Swimming Ability of Young Rats

1981

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Neonatal swimming behavior was studied after a single subcutaneous injection of L-dopa methyl ester (50 mg/kg; 200 mg/kg) apomorphine (0.1 mg/kg; 1.0. mg/kg), DL-amphetamine (0.5 mg/kg; 10 mg/kg), haloperidol (0.5 mg/kg; 1.0 mg/kg), L-tryptophan (50 mg/kg; 100 mg/kg), methysergide (1.0 mg/kg; 5.0 mg/kg) as well as intraventricular injection of 100 µg 6-OHDA. 1-, 3-, 5- and 7-day-old rats were placed into a temperature-controlled aquarium (37°C) and the pattern of motor coordination, latency time to swimming (LTS) and the number of foreleg strokes for 10 s (FS) were measured. When compared to the physiological saline-injected controls, rats that received L-dopa showed a striking increase of FS at all ages but the most striking improvement of motor coordination was found in newborn rats. On day 1 both doses of DL-amphetamine induced increases in FS and improvement of motor coordination, whereas apomorphine failed to show any effect at this age. On days 3, 5 and 7 low doses of DL-amphetamine and apomorphine increased the FS. However, high doses resulted in a decrement in swimming performance. Haloperidol impaired swimming on day 1 but produced a significant increase of FS on days 5 and 7. Neonatal injection of 6-OHDA delayed development of motor coordination, reduced FS and increased LTS. On days 3,5 and 7 high doses of L-tryptophan elicited an increase of FS, while high doses of methysergide caused significant impairment of performance. It is suggested that the brain rapidly converts the administered L-dopa to dopamine during the first week of life and there appears to be a strong dependent relationship between the pattern of motor coordination and the amount of available dopamine in the developing brain.

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“…Metergoline (MCE), an ergoline derivative with strong peripheral [2] and central antiserotoninergic activity [12,19,37], has been shown to inhibit prolactin (Prl) release after acute or short-term administration in normal subjects [14,15,36], in puerperal women [8], and in several hyperprolactinemicpatients [13]. The Prl responses to thyrotropin-releasing hormone (TRH) [15] and to the dopa-decarboxylase inhibitor Ro4-4602 [36] are also in hibited by the drug in healthy persons.…”

mentioning

confidence: 99%

Restoration of the Prolactin Response to Sulpiride by Metergoline Administration in Hyperprolactinemic Patients

et al. 1979

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Although metergoline (MCE) inhibits prolactin (Prl) secretion in normal and hyperprolactinemic subjects similarly to dopamine (DA) and DA agonists, several data suggest that it acts through a different mechanism, probably as a serotonin antagonist. To further evaluate its Prl-lowering effect, paired sulpiride (Sulp) tests (100 mg i.m.) were performed before and after acute MCE administration (4 mg by mouth 120 min before Sulp) in 10 normal women, while 30 hyperprolactinemic women with pituitary microadenoma and no Prl response to Sulp were studied before and after acute or chronic treatment with either MCE (8–12 mg/day for 1-3 months) or bromocriptine (CB-154) (2.5 mg 300 min before Sulp, or 5 mg/day for 1-2 months), or during DA infusion (5 μg/kg/min for 180 min, Sulp being injected at 120 min). MCE did not alter the Sulp-stimulated Prl release in normal subjects and induced, both after acute and chronic administration, a clear Prl response to Sulp in hyperprolactinemic patients, which did not differ from that occurring in normals. During DA infusion, Sulp induced a marked increase in serum Prl levels, as previously reported in hyperprolactinemic patients without evidence of pituitary tumor; this increase was significantly higher than that observed in normals and in MCE-treated hyperprolactinemic subjects. No Prl response to Sulp occurred in CB-154-treated patients. Basal Prl levels were significantly lowered by all treatments. Although the similarity of effects of MCE and DA on Sulp-induced Prl release might suggest that MCE acts by stimulation of DA receptors, this hypothesis is not supported by pharmacological nor by in vitro and in vivo endocrinological studies; such an action might perhaps be exerted by the drug indirectly via serotoninergic blockade or through hypothetical metabolites. Alternatively, MCE might induce a Prl increase after Sulp in hyperprolactinemic patients by restoring the response of the normal lactotropes, usually suppressed by a central dopaminergic

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STIMULATORY EFFECT OF THE DOPA-DECARBOXYLASE INHIBITOR Ro 4-4602 ON PROLACTIN RELEASE; INHIBITION BY L-DOPA, METERGOLINE, METHYSERGIDE AND 2-Br-α-ERGOCRYPTINE

Cited by 29 publications

References 19 publications

Lack of Counteracting Effect of Liposomes on Benserazide-Induced Hyperprolactinemia

Lack of Counteracting Effect of Liposomes on Benserazide-Induced Hyperprolactinemia

The Role of Dopaminergic and Serotonergic Mechanisms in the Development of Swimming Ability of Young Rats

Restoration of the Prolactin Response to Sulpiride by Metergoline Administration in Hyperprolactinemic Patients

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