On the role of dopamine receptors in the central regulation of human TSH

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.).

Section: Discussionsupporting

confidence: 71%

Morphine-Induced TSH Release in Normal and Hypothyroid Subjects

Devilla¹,

Pende²,

Morgano³

et al. 1985

“…This to gether with a relatively large interindividual variability may perhaps explain several negative results [43,50,91,124], Hard to fit into this general framework is the report of Collu et al [17] that pimozide, another DA receptor blocker caused a marked decrease of TSH levels in euthyroid sub jects. Colin's results were, however, not corroborated by a recent study [19] showing that the classical dopamine recep tor blockers pimozide or haloperidol are as effective as the substituted benzamides metoclopramide or sulpiride in stimulating TSH secretion in humans.…”

Section: Dopaminementioning

confidence: 66%

“…18, 52, 61.69] regard less of the thyroid status of the subject. The effect of do pamine could be abolished by administration of the dopa mine receptor antagonist domperidone [19], A counterpart to studies with dopaminergic agonists is a series of reports based on the use of blockers of the dopa mine receptors. Sowers et al [122] were probably the first to describe a slight elevation of serum TSH levels in euthyroid men following administration of metoclopramide.…”

Section: Dopaminementioning

confidence: 99%

Neurotransmitter Control of Thyrotropin Secretion

Krulich

1982

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.

“…At present, DA receptors at the thyrotrophic cell level are not known. Non etheless, since domperidone, which also seems not to cross the blood-brain barrier [17], determines a TSH increase [7,23], it is possible to hypothesize the presence of an action site both at the median eminence and hypophyseal level. The absent effect of NOM on PRL secretion in our normoprolactinemic subjects ( fig.…”

Section: Discussionmentioning

confidence: 99%

“…In addi tion, DA receptor blocking drugs such as sulpiride [20], metoclopramide [32], pimozide [7] and domperidone [7] have been shown to stimulate TSH release.…”

mentioning

confidence: 99%

The Effect of Nomifensine on Thyroid-Stimulating Hormone (TSH) in Normal and Hyperprolactinemic Subjects

Giusti¹,

Mazzocchi²,

Mignone³

et al. 1983

Thyroid-stimulating-hormone (TSH) secretion was studied in 28 normal subjects (12 males; 16 females) and in 8 subjects with prolactin (PRL) secreting tumors (1 male; 7 females) after nomifensine (NOM) administration (200 mg orally). NOM is a drug which activates dopaminergic (DA) neurotransmission at the central nervous system level. Blood samples were drawn every hour for 4 h after NOM or placebo administration. On the 4th h thyrotrophin-releasing-hormone (TRH) was administered in bolus (200 μg i.v.), to both groups, and additional samples were collected at 10-, 20-, 30-, 60-and 90-min intervals. The results indicate that in normal subjects, but not in prolactinomas, NOM induces a moderate but significant reduction in TSH secretion. Furthermore, the TSH response to TRH was found to be significantly reduced. No variation was discerned, however, in PRL secretion after NOM. The hormone response to TRH remained unaffected. The data confirm that in normal subjects the DA neurotransmission exerts an inhibitory role upon TSH secretion. In subjects affected by prolactinomas, an alteration in central DA availability may be hypothesized.