Domperidone, an Extracerebral Inhibitor of Dopamine Receptors, Stimulates Thyrotropin and Prolactin Release in Man

Delitala, G.; Devilla, L.; Lotti, G

doi:10.1210/jcem-50-6-1127

Cited by 41 publications

(17 citation statements)

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“…Comparing morphine data with those obtained with dopamine antaggonists administration it is possible to observe similar ef fects with regard both to the degree of TSH increase, lower than that of PRL, and to enhancement of the TSH response to TRH [4,6]. Moreover, our preliminary data (not re ported) show that bromocriptine, a dopamine agonist, is able to blunt morphine-induced TSH and PRL release.…”

Section: Discussionsupporting

confidence: 71%

Morphine-Induced TSH Release in Normal and Hypothyroid Subjects

Devilla¹,

Pende²,

Morgano³

et al. 1985

Neuroendocrinology

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The effects of morphine (10 mg i.v.), an opioid agonist, and of naloxone (10 mg i.v.), an opioid antagonist, on serum levels of TSH and PRL were studied in 7 hypothyroid patients and in 5 normal volunteers. Morphine administration induced a prompt, significant increase in serum TSH and PRL in all subjects. The degree of PRL release after morphine was similar in the two groups, while, as regards TSH, the increase was more evident in hypothyroid subjects. Pretreatment with naloxone (4 mg i.v. 5 min before morphine administration) blocked these effects in all subjects. In contrast, naloxone alone was not able to affect significantly TSH and PRL secretion. Moreover, in 5 other euthyroid volunteers, morphine significantly enhanced the response of TSH and PRL to TRH stimulation (200 µg i.v.).

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Section: Discussionsupporting

confidence: 71%

Morphine-Induced TSH Release in Normal and Hypothyroid Subjects

Devilla¹,

Pende²,

Morgano³

et al. 1985

Neuroendocrinology

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“…Sowers et al [122] were probably the first to describe a slight elevation of serum TSH levels in euthyroid men following administration of metoclopramide. Their re sults were subsequently confirmed and expanded by other workers using metoclopramide [41,109,110], the related drug sulpiride [68,143] or the novel blocker, domperidone [20,67,94]. It soon became evident that the magnitude of the rise in the TSH levels is determined by several factors.…”

Section: Dopaminementioning

confidence: 74%

Neurotransmitter Control of Thyrotropin Secretion

Krulich

1982

Neuroendocrinology

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The central dopaminergic system seems to have an inhibitory influence on the secretion of thyrotropin (TSH) both in humans and rats. This is documented by observations that in humans, especially in subjects with primary hypothy-roidism, the dopamine precursor l-Dopa, dopamine receptor agonist bromocryptine, and dopamine itself decrease plasma levels of TSH and in some instances inhibit TSH secretory response to thyrotropin-releasing hormone (TRH). Conversely blockade of dopamine receptors leads to an elevation of circulating TSH. It is probable the dopaminergic drugs act on the pituitary thyrotrops rather than on the release of hypothalamic TRH. Analogous results were obtained in rats. In contrast, the noradrenergic system, studied mainly in rats, has a stimulatory influence on the secretion of TSH. This view is mainly supported by findings that acute interruption of noradrenergic neurotransmission causes a decrease of serum TSH levels and blocks the cold-induced stimulation of TSH secretion. The role of the central serotonergic system remains undecided because some experimental findings indicate that it has an inhibitory influence but others indicate an opposite function. The remaining transmitter systems have not been studied extensively enough to allow definite conclusions about their roles in the regulation of TSH secretion.

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“…Separate studies with intramuscular or oral domperidone indicated that the drug had the same potency as metoclopramide in inducing prolactin release. [102][103][104] Based on these findings, it is unlikely that the different prolactin levels caused by the various antagonists are due to different affinities at the dopamine D 2 receptor, as domperidone and clebopride have comparable affinities (see Table 1) 1 . It is also unlikely that the various antagonists can differently modulate the release of dopamine from the tuberoinfundibular pathway, as dopamine D 2 autoreceptors are absent in this pathway.…”

Section: Hyperprolactinaemiamentioning

confidence: 98%

Clinical implications of enteric and central D₂ receptor blockade by antidopaminergic gastrointestinal prokinetics

Tonini

Cipollina

Poluzzi

et al. 2004

Aliment Pharmacol Ther

255

207

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SUMMARYAntidopaminergic gastrointestinal prokinetics (bromopride, clebopride, domperidone, levosulpiride and metoclopramide) have been exploited clinically for the management of motor disorders of the upper gastrointestinal tract, including functional dyspepsia, gastric stasis of various origins and emesis. The prokinetic effect of these drugs is mediated through the blockade of enteric (neuronal and muscular) inhibitory D 2 receptors. The pharmacological profiles of the marketed compounds differ in terms of their molecular structure, affinity at D 2 receptors, ability to interact with other receptor systems [5-hydroxytryptamine-3 (5-HT 3 ) and 5-HT 4 receptors for metoclopramide; 5-HT 4 receptors for levosulpiride) and ability to permeate the bloodbrain barrier (compared with the other compounds, domperidone does not easily cross the barrier). It has been suggested that the serotonergic (5-HT 4 ) component of some antidopaminergic prokinetics may enhance their therapeutic efficacy in gastrointestinal disorders, such as functional dyspepsia and diabetic gastroparesis. The antagonism of central D 2 receptors may lead to both therapeutic (e.g. anti-emetic effect due to D 2 receptor blockade in the area postrema) and adverse (including hyperprolactinaemia and extrapyramidal dystonic reactions) effects. As the pituitary (as well as the area postrema) is outside the blood-brain barrier, hyperprolactinaemia is a side-effect occurring with all antidopaminergic prokinetics, although to different extents. Extrapyramidal reactions are most commonly observed with compounds crossing the blood-brain barrier, although with some differences amongst the various agents. Prokinetics with a high dissociation constant compared with that of dopamine at the D 2 receptor (i.e. compounds that bind loosely to D 2 receptors in the nigrostriatal pathway) elicit fewer extrapyramidal signs and symptoms. A knowledge of central and peripheral D 2 receptor pharmacology can help the clinician to choose between the antidopaminergic prokinetics to obtain a more favourable risk/ benefit ratio.

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Domperidone, an Extracerebral Inhibitor of Dopamine Receptors, Stimulates Thyrotropin and Prolactin Release in Man

Cited by 41 publications

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Morphine-Induced TSH Release in Normal and Hypothyroid Subjects

Morphine-Induced TSH Release in Normal and Hypothyroid Subjects

Neurotransmitter Control of Thyrotropin Secretion

Clinical implications of enteric and central D₂ receptor blockade by antidopaminergic gastrointestinal prokinetics

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Domperidone, an Extracerebral Inhibitor of Dopamine Receptors, Stimulates Thyrotropin and Prolactin Release in Man

Cited by 41 publications

References 0 publications

Morphine-Induced TSH Release in Normal and Hypothyroid Subjects

Morphine-Induced TSH Release in Normal and Hypothyroid Subjects

Neurotransmitter Control of Thyrotropin Secretion

Clinical implications of enteric and central D2 receptor blockade by antidopaminergic gastrointestinal prokinetics

Contact Info

Product

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Clinical implications of enteric and central D₂ receptor blockade by antidopaminergic gastrointestinal prokinetics