Evidence for Dopaminergic Control of Thyrotrophin Secretion in Man

Scanlon, M. F.; Mora, B.; Shale, Dennis J.; Hall, R.; Weightman, D.; Heath, Martha E.; Snow, Michael

doi:10.1016/s0140-6736(77)90607-9

Cited by 85 publications

(45 citation statements)

References 12 publications

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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: 75%

“…Another factor is the thyroid status. Pa tients with primary hypothyroidism display a larger in crease than euthyroid controls [68,110], Within the hypo thyroid group the TSH response is inversely related to the severity of the condition [31, 105,110], Another determinant is possibly time of the day, because, according to Scanlon et al [108], the TSH release is more pronounced at the acrophase (around 23.00 h) of the human TSH daily rhythm than at its nadir (around 11.30 h). Finally, a greater reaction was observed in patients with hyperprolactinemia [69,95] which may reflect changes in metabolism of dopamine due to sustained elevation of prolactin levels.…”

Section: Dopaminementioning

confidence: 99%

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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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Section: Dopaminementioning

confidence: 75%

Section: Dopaminementioning

confidence: 99%

Neurotransmitter Control of Thyrotropin Secretion

Krulich

1982

Neuroendocrinology

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“…Electroconvulsive treatment also eli cits in humans a rise in serum prolactin, adrenocortotropic hormone (ACTH), and thyrotropin [4,20,21,23]. The re lease of prolactin and thyrotropin is stimulated by thyrotro pin-releasing hormone (TRH) (13] and inhibited by dopa mine [13,15,32], Norepinephrine, melatonin, and serotonin also influence the release of pituitary hormones [13,27,30,33]. A cortisol increase after seizure [8,19,21] was con sidered to be a 'nonspecific stress' response [II].…”

mentioning

confidence: 99%

Epileptic but Not Psychogenic Seizures Are Accompanied by Simultaneous Elevation of Serum Pituitary Hormones and Cortisol Levels

Rao

Stefan²,

Bauer³

1989

Neuroendocrinology

101

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The circadian rhythm of serum prolactin was determined in 12 patients with seizures, and 28 age- and sex-matched healthy subjects (14 men and 14 women). Blood was also collected every 15 min for 2 h immediately after a simultaneously video/EEG-documented epileptic (6 patients) and psychogenic seizure (5 patients) for the determination of prolactin, thyrotropin, growth hormone, cortisol, melatonin, catecholamines and serotonin. During the seizure-free interval, the circadian profile of serum prolactin was lower in female patients than in healthy women. Serum prolactin, thyrotropin, growth hormone, and cortisol were increased postictally, followed by a decrease, after a grand mal or complex partial seizure, but not after a psychogenic seizure in comparison to baseline serum hormone levels obtained during the same time on a seizure-free day. During the seizure and for 2 h afterwards, blood serotonin, serum melatonin, dopamine, and epinephrine did not alter and were within the reference limits of healthy subjects. Serum norepinephrine was lower in patients compared to healthy subjects (p < 0.05). The simultaneous elevation of serum prolactin, thyrotropin, growth hormone, and cortisol points to a central stimulation of the hypothalamic-pituitary axis during an epileptic seizure, but not during seizures of psychogenic origin.

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“…Unasso ciated a-sub and TSH-p may be found circulating 'free' into the blood stream as a result of direct pituitary secretion and not of Received: July 30, 1990 Accepted after revision: October 3, 1990 TSH peripheral catabolism [4]. Moreover, a-sub levels in pe ripheral blood parallel the levels of LH and FSH, increasing from puberty to adulthood and following gonadotropin rhyth mic fluctuations [5,6).Circulating free thyroid hormones and several hypothalamic factors, in particular thyrotropin-releasing hormone (TRH) and dopamine (DA), modulate the synthesis and secretion of holo-TSH and its subunits [7][8][9], Studies on subunit mRNA levels in cultured pituitary cells have demonstrated that the above factors regulate the transcription rate of both subunit genes, and that their action on the expression of a-sub and TSH-p genes may be discordant [10][11][12][13].Although much is known about the regulation of holo-TSH secretion, few studies about TSH subunit responses to TRH and …”

mentioning

confidence: 99%

Thyrotropin Alpha- and Beta-Subunit Responses to Thyrotropin-Releasing Hormone and Domperidone in Normal Subjects and in Patients with Microprolactinomas

et al. 1991

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Microprolactinoma is a particular pathological situation characterized by the presence of increased hypothalamic dopaminergic tone reactive to tumoral hyperprolactinemia. Since dopamine (DA) is a physiological regulating factor of the secretion of thyroid-stimulating hormone (TSH), we investigated the responses of serum TSH (holo-TSH) and its subunits (α-subunit: α-sub, and TSH-β) to thyrotropin-releasing hormone (TRH) and domperidone (DOM; an antidopaminergic drug acting outside the blood-brain barrier) in 36 euthyroid subjects (20 controls and 16 patients with microprolactinoma) in order to evaluate the possible in vivo effects of DA excess on TSH subunit secretion. No significant difference in serum TSH increase after TRH (200 µg i.v.) was observed between patients with microprolactinoma and controls (TSH net incremental area under the curve, nAUC: 146 ± 9, mean ± SE, and 143 ± 7.7 µg/1/60 min, respectively), while serum α-sub and TSH-β responses were markedly reduced in patients with microprolactinoma as compared to those found in normals (α-sub nAUC: 3.0 ± 0.5 vs. 19.8 ± 2.2 µg/1/60 min, p < 0.001; TSH-β nAUC: 5.0 ± 0.8 vs. 9.5 ± 0.9 µg/1/60 min, p < 0.05). Serum TSH response to DOM administration (10 mg i.v.) was significantly higher in patients with microprolactinoma than in controls (TSH nAUC: 76 ± 12.7 vs. 28 ± 8.3 µg/1/90 min, p < 0.001), while serum α-sub increase was similar in the two groups (α-sub nAUC: 8.7 ± 4.8 and 10.2 ± 4.7 µg/1/90 min, p = NS), and serum TSH-β did not show any increase in patients with microprolactinoma (TSH-β nAUC: 0.2 ± 0.1 vs. 6.0 ± 3.3 µg/1/90 min, p < 0.001). The present findings show that in normal subjects, α-sub and TSH-β are cosecreted along with holo-TSH in response to both TRH and dopaminergic receptor blockade by DOM. On the contrary, in patients with microprolactinoma, α-sub and TSH-β responses to the above stimulatory agents are definitely impaired. Such an impairment is particularly evident after DOM administration which caused a holo-TSH release 3-fold higher than in controls. The discrepancy between the secretory response of holo-TSH and that of both α-sub and TSH-β in the condition of increased hypothalamic dopaminergic tone suggests a preferential secretion of holo-TSH molecules in order to overcome the chronic dopaminergic inhibition and maintain normal thyroid stimulation.

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Evidence for Dopaminergic Control of Thyrotrophin Secretion in Man

Cited by 85 publications

References 12 publications

Neurotransmitter Control of Thyrotropin Secretion

Neurotransmitter Control of Thyrotropin Secretion

Epileptic but Not Psychogenic Seizures Are Accompanied by Simultaneous Elevation of Serum Pituitary Hormones and Cortisol Levels

Thyrotropin Alpha- and Beta-Subunit Responses to Thyrotropin-Releasing Hormone and Domperidone in Normal Subjects and in Patients with Microprolactinomas

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