Some current aspects of clinical and experimental neuroendocrinology with particular reference to growth hormone, thyrotropin and prolactin

Scanlon, M. F.; Pourmand, M.; McGregor, A.M.; Rodríguez-Arnao, M. D.; Hall, K.; Gómez-Pan, A.; Hall, R.

doi:10.1007/bf03350424

Cited by 50 publications

(22 citation statements)

References 219 publications

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“…The participation of the dopaminergic pathways in the control of GH release has been clearly documented in man [18]. It is well known that DA agonist drug administration induces an increase of serum GH concentration [10].…”

Section: Discussionmentioning

confidence: 99%

“…Activation of central nervous system (C. N. S.) cholinergic pathways enhances GH secretion and the administration of gabaergic compounds has a stimulatory effect on GH release. In rat, opioid peptides have been reported to stimulate GH secretion, and in man the administration of an analogue of metenkefaline (FK 33 -084) was effective in increasing serum GH concentrations [10,18]. The regulation of GH secretion during fetal life or in the perinatal period has been less extensively studied.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Dopaminergic regulation of fetal growth hormone (GH) secretion: study with maternal administration of bromocriptine

Robuschi¹,

Montermini²,

Chiodera³

et al. 1987

Journal of Perinatal Medicine

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Dopaminergic regulation of fetal growth hormone (GH) secretion: study with maternal administration of bromocriptine

Robuschi¹,

Montermini²,

Chiodera³

et al. 1987

Journal of Perinatal Medicine

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“…In vivo the effects of dopamine agonists and an tagonists occur promptly and do not require prolonged ex posure to the drugs [13][14][15].…”

Section: Discussionmentioning

confidence: 99%

“…The physiological role of dopamine in the control of thy roid-stimulating hormone (TSH) release is unclear and stu dies in man using dopamine, dopamine agonists and antago nists have given conflicting evidence which has been exten sively reviewed [13][14][15]. However, recent evidence both in euthyroid [I, 3, 7, 10, 16, 19] and hypothyroid individuals [3,4] would seem to establish dopamine as having an inhibi tory role in the release of TSH.…”

mentioning

confidence: 99%

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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“…Metoclopramide (MCP), a dopamine (DA) antagonist, acutely stimulates prolactin and aldosterone secretion in man [Sowers et al" 1976[Sowers et al" , 1980Norbiato et al, 1977;Carey et al, 1979], The aldosterone stimulating action of MCP is presumably mediated by its antagonist activity at central or peripheral DA receptors [Carey et al, 1980], Patients with hyperprolactinemia caused by microprolactinomas show a loss or a re duction of dopaminergic inhibition of PRL release and an increase in dopaminergic in hibition of TSH release [Scanlon et al, 1979[Scanlon et al, , 1981Quigley and Yen, 1980;Spitz et al. 1983].…”

mentioning

confidence: 99%

Plasma Aldosterone Response to Metoclopramide Is Unmodified by Hyperprolactinemia

Serri¹

1987

Horm Res

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It has been previously demonstrated that patients with hyperprolactinemia have impaired PRL response to dopaminergic blockade and increased TSH response. Since inhibitory dopaminergic modulation of aldosterone is well established, we have examined whether prolactinoma patients have an altered aldosterone response to dopaminergic blockade. To investigate this possibility we compared the plasma PRL, TSH and aldosterone responses to the dopamine (DA) antagonist metoclopramide (MCP; 10 mg i.v.) in 10 women with prolactinomas and 7 healthy female controls. Basal PRL levels in prolactinoma patients were elevated and showed a blunted rise following MCP. Although basal TSH levels were similar in the 2 groups of subjects, they significantly increased (p = 0.017) in prolactinoma patients while in contrast they did not significantly change in control subjects. Basal supine plasma aldosterone was similar in patients with prolactinomas (0.23 ± 0.03 nmol/l) and in healthy subjects (0.25 ± 0.04 nmol/l) and the increased aldosterone concentrations from 15 to 120 min following MCP were not significantly different in prolactinoma patients and in control subjects. It is concluded that in patients with prolactinomas, the alteration in the dopaminergic regulation is specifically related to the lactotroph.

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Some current aspects of clinical and experimental neuroendocrinology with particular reference to growth hormone, thyrotropin and prolactin

Cited by 50 publications

References 219 publications

Dopaminergic regulation of fetal growth hormone (GH) secretion: study with maternal administration of bromocriptine

Dopaminergic regulation of fetal growth hormone (GH) secretion: study with maternal administration of bromocriptine

Dopaminergic Control of the Rat Thyrotroph

Plasma Aldosterone Response to Metoclopramide Is Unmodified by Hyperprolactinemia

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