Bromocriptine Suppression of the Thyrotrophin Response to Thyrotrophin Releasing Hormone

Yap, P. L.; Davidson, Neil; Lidgard, Graham P.; Fyffe, J. A.

doi:10.1111/j.1365-2265.1978.tb02196.x

Cited by 35 publications

(18 citation statements)

References 19 publications

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“…It has been suggested that in the rat the principal site of action is suprapituitary since do pamine agonists were shown to have no effect on TSH re lease in response to exogenous thyrotrophin-releasing hor mone (TRH) [12]. This is at variance with the situation in man where TRH-stimulated TSH release has been demon strated to be under dopaminergic inhibition [1,16,19]. Re cent studies utilising rat pituitary cells in culture have de monstrated a direct action of dopamine on pituitary cells [5] although preliminary data from our laboratory had indicat ed that this was not the case [Yeo a n d Besser, unpublished observations].…”

contrasting

confidence: 51%

Dopaminergic Control of the Rat Thyrotroph

Price¹,

Grossman

Besser

et al. 1983

Neuroendocrinology

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The established technique of dynamic perfusion of dispersed rat anterior pituitary cells was used to investigate the role of dopamine in the release of thyroid-stimulating hormone (TSH). The basal release of TSH was 124 ± 22 ng/ml (mean ± SEM) and this remained unchanged in the presence of dopamine (5 × 10^–6M), while basal prolactin release was suppressed to 50% of control values. Perfusion with thyrotrophin-releasing hormone (TRH) in doses between 1.4 × 10^–10 and 22.4 × 10^–10M produced a consistent and reproducible dose-response curve for TSH (n = 14) which was not significantly altered by the presence of dopamine (n = 5). Perfusion with bromocriptine (10^–6M), a dopamine agonist, did not alter the basal or stimulated TSH release. No stimulation of TSH release was observed when the cells were challenged with 2-min pulses of domperidone, a dopamine antagonist (2 × 10^–9 to 2 × 10^–5M). The inclusion of somatostatin-14 (3 × 10^–9 M) in the perfusate inhibited TRH-stimulated TSH release. Our results suggest that, in the rat, dopaminergic inhibition of TSH release does not occur at the level of the pituitary.

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contrasting

confidence: 51%

Dopaminergic Control of the Rat Thyrotroph

Price¹,

Grossman

Besser

et al. 1983

Neuroendocrinology

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“…The secretion of TSH is further modulated by neuropeptides such as somatostatin, and neurotrans mitters such as dopamine and gamma-aminobutyric acid (GABA) [3][4][5].…”

Section: Introductionmentioning

confidence: 99%

Gamma-Aminobutyric Acid and Dysregulation of TSH Secretion in Uremic Male Rats

Elias¹,

Vaziri²,

Pandian³

et al. 1987

Nephron

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The role of gamma-aminobutyric acid (GABA) in the abnormal secretion of thyrotropic hormone (TSH) in uremia was studied in male Sprague-Dawley rats rendered renally insufficient by subtotal nephrectomy. Baseline TSH concentrations in normal control animals and in the uremic animals were similar. The peak TSH response to thyrotropin-releasing hormone (TRH; 5 μg i.v.) was significantly blunted in the uremic animals compared to the controls. Pretreatment of the uremic animals with the specific GABA antagonist, bicuculline (1.5 μmol i.v.) resulted in normalization of the peak TSH response to TRH. Bicuculline pretreatment, however, did not alter the basal secretion of TSH in either the normal or the uremic animals, and it also did not augment the TRH-stimulated TSH response in the normal animals. Sham-operated animals demonstrated basal and TRH-stimulated TSH responses comparable to the control group. In order to assess whether the weight loss associated with uremia could have accounted for the blunted TRH-stimulated TSH secretion in the uremic animals, a group of rats were starved so that their weights were comparable to those of the uremic animals. Basal and TRH-stimulated TSH responses in this group were not significantly different from the controls. Bicuculline pretreatment of the starved animals also failed to alter the basal and TRH-stimulated TSH responses. These data indicate that an increase in central gabaergic tone may be partly responsible for the blunted TSH response to TRH seen in uremia, but that GABA is not an important modulator of TSH secretion in the normal rat.

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“…Administration of octreotide or bromocriptine inhibits TSH secretion [7,8,13], but altered thyroid function in the present case may not be due to TSH secretion, since TSH levels were always suppressed.…”

Section: Discussionmentioning

confidence: 96%

“…In most studies, serum T4i ]T3 and basal TSH levels are found to be normal. Both octreotide and bromocriptine are used to treat acromegaly, and acute administration of these drugs is reported to suppress TSH secretion [7,8], but chronic treatment with octreotide or bromocriptine did not alter thyroid function in most patients with acromegaly [9][10][11].…”

Section: In Acromegalicmentioning

confidence: 99%

Octreotide and Bromocriptine Suppress Thyroid Hormone Levels and Thyroid Nodule in an Acromegalic Patient with Nontoxic Autonomous Goiter.

et al. 1997

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Abstract.An acromegalic patient with nontoxic autonomous goiter was sequentially treated with octreotide and bromocriptine. Before therapy, serum GH, PRL and insulin-like growth factor-I (IGF-I) levels were increased.Free T3 and free T4 were within the normal range with suppressed TSH levels, whereas 123Iodine-uptake of thyroid was 5.6% after 24 h. During treatment with octreotide and bromocriptine, serum GH, PRL, and IGF-I became normal and free T3 and free T4 were slightly but significantly decreased, but TSH levels remained very low. After thyroidectomy, thyroglobulin, free T3 and free 14 were further decreased, and the TSH levels were recovered to normal. These findings suggested that octreotide and bromocriptine inhibit the release of thyroid hormones from the autonomous thyroid gland directly or indirectly through the decline in IGF-I.

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Bromocriptine Suppression of the Thyrotrophin Response to Thyrotrophin Releasing Hormone

Abstract: A single oral dose of 5 mg of bromocriptine significantly lowered the TSH response to 200 microgram TRH intravenously in eight healthy men compared with control experiments in the same subjects. This finding may be relevant in chronic bromocriptine therapy.

Cited by 35 publications

References 19 publications

Dopaminergic Control of the Rat Thyrotroph

Dopaminergic Control of the Rat Thyrotroph

Gamma-Aminobutyric Acid and Dysregulation of TSH Secretion in Uremic Male Rats

Octreotide and Bromocriptine Suppress Thyroid Hormone Levels and Thyroid Nodule in an Acromegalic Patient with Nontoxic Autonomous Goiter.

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