STIMULATING ACTION OF SULPIRIDE AND PIMOZIDE ON PROLACTIN RELEASE EFFECT ON BROMOCRIPTINE, L-DOPA AND METERGOLINE ADMINISTRATION

ABSTRACT In order to evaluate the mechanism of action of metergoline, an antiserotonin agent, the effect of pre-treatment with metergoline on prolactin (PRL) release induced by sulpiride was compared to that obtained after bromocriptine administration in normal subjects. In addition, the metergoline effect on PRL release induced by pimozide, specific dopamine receptor blocking agent, was compared to that obtained with L-dopa. Metergoline administration resulted in definite decrease in plasma PRL in all subjects; however, metergoline did not block, differently from bromocriptine, the PRL release induced by sulpiride. On the contrary, metergoline, like L-dopa, inhibited PRL release induced by pimozide pre-treatment. These results raise the possibility that metergoline does not act as an antiserotonin agent; its antilactogenic effect observed under basal conditions may be dependent on different mechanisms of action.

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Effect of [Asu,]eel calcitonin on prolactin release in normal subjects and patients with prolactinoma

Acta Endocrinologica ◽

10.1530/acta.0.1080297 ◽

1985 ◽

Vol 108 (3) ◽

pp. 297-304 ◽

Cited By ~ 6

Author(s):

Hidesuke Kaji ◽

Kazuo Chihara ◽

Naoto Minamitani ◽

Hitoshi Kodama ◽

Tetsuya Kita ◽

...

Keyword(s):

Body Weight ◽

Bolus Injection ◽

Normal Subjects ◽

Regular Insulin ◽

Prolactin Release ◽

Saline Administration ◽

The Central Nervous System ◽

Plasma Prl ◽

Male Subjects

Abstract. The effect of [Asu]eel calcitonin (ECT), an equipotent analogue of eel CT, on prolactin (Prl) secretion was examined in 12 healthy male subjects and in 6 patients with prolactinoma. In healthy subjects, ECT (0.5 μg/kg body weight · h) or saline was infused for 2 h and TRH was injected iv as a bolus of 500 μg at 1 h of ECT or saline administration. ECT did not affect basal Prl levels during 1 h of infusion. TRH caused a significant increase of plasma Prl with peak values of 75.2 ± 11.6 ng/ml in ECT-infused subjects, which did not differ from those infused with saline (68.5 ± 8.3 ng/ml). Next, an iv bolus injection of regular insulin (0.1 U/kg body weight) was followed by an infusion of ECT or saline alone. Plasma Prl peaks after hypoglycaemic stress were significantly lower in ECT-infused subjects than those in saline-injected controls (ECT, 16.5 ± 3.1 vs 33.5 ± 9.6 ng/ml, P < 0.05). In patients with prolactinoma, basal levels of plasma Prl ranging from 42.0–4130 ng/ml failed to change during iv infusion of ECT. Moreover, ECT (10−9–10−6m) did not affect Prl release from prolactinoma tissues perifused in vitro. These findings suggest that ECT may not act directly on the pituitary to modify Prl release. Rather, peripherally administered ECT appears to suppress Prl release via the central nervous system.

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Dopamine-receptor blocking agent-associated akathisia: a summary of current understanding and proposal for a rational approach to treatment

Therapeutic Advances in Psychopharmacology ◽

10.1177/2045125320937575 ◽

2020 ◽

Vol 10 ◽

pp. 204512532093757

Author(s):

Shaina Musco ◽

Vivian McAllister ◽

Ian Caudle

Keyword(s):

Dopamine Receptor ◽

Blocking Agent ◽

Population Based ◽

Rational Approach ◽

Receptor Blocking ◽

Serotonergic Receptors ◽

Vulnerable Patient ◽

The Subject ◽

Dopamine Signaling ◽

The Brain

Dopamine-receptor blocking agent-associated akathisia (DRBA-A) is an adverse effect that can significantly limit the use of these important medications for the treatment of a variety of psychiatric diseases, yet there is no unifying theory regarding its pathophysiology. This knowledge gap limits clinicians’ ability to effectively manage DRBA-A and mitigate negative outcomes in an already vulnerable patient population. Based on a review of the current literature on the subject, it is hypothesized that dopaminergic and noradrenergic signaling is perturbed in DRBA-A. Accordingly, it is proposed that the optimal agent to manage this extrapyramidal symptom should increase dopamine signaling in the affected areas of the brain and counteract compensatory noradrenergic signaling via antagonism of adrenergic or serotonergic receptors.

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Hyperprolactinaemia and DNA synthesis in the pituitary gland of the rat

Journal of Endocrinology ◽

10.1677/joe.0.0970065 ◽

1983 ◽

Vol 97 (1) ◽

pp. 65-74 ◽

Cited By ~ 6

Author(s):

J. A. Burdman ◽

M. T. Calabrese ◽

R. M. MacLeod

Keyword(s):

Dna Synthesis ◽

Pituitary Gland ◽

Dopamine Receptor ◽

Dna Content ◽

Anterior Pituitary ◽

Blocking Agent ◽

Anterior Pituitary Gland ◽

Host Animal ◽

Receptor Blocking ◽

Tumour Bearing

Hyperprolactinaemia produced in rats by the transplanted prolactin-secreting tumours MtTW15 and 7315a significantly (P<0·01) inhibited by 70% the incorporation of [3H]thymidine into the pituitary DNA of the host animals. The weight and the DNA content of the glands were significantly (P<0·01) reduced by 30%. The administration of haloperidol, a dopamine receptor blocking agent, to the tumour-bearing rats increased the suppressed DNA replication in the anterior pituitary glands by approximately 560% in the MtTW15-bearing rat and by 100% in the 7315a-bearing animals. Furthermore, injection of drugs which stimulate prolactin release either by blocking the synthesis of dopamine (α-methyl-p-tyrosine) or the re-uptake of dopamine (reserpine) stimulated DNA synthesis by 800 and 100% respectively in the anterior pituitary gland of rats bearing the MtTW15 tumour. In contrast, lisuride, a dopamine agonist, significantly inhibited the incorporation of [3H]thymidine into the DNA of the pituitary gland of normal but not hyperprolactinaemic rats. Chronically administered oestrogens to hyperprolactinaemic rats increased the weight (100%), DNA content (31%), incorporation of [3H]thymidine into DNA (680%) and synthesis and release of prolactin (300%) in the pituitary gland. The incorporation of [3H]thymidine into tumour DNA was several times higher than in the pituitary gland of the host animal and was not significantly modified by any of the above treatments. Likewise the hyperprolactinaemia of the tumour-bearing rats was not significantly changed. In conclusion, we have shown that hyperprolactinaemia inhibits DNA synthesis in the anterior pituitary gland and this inhibition can be reversed completely by a dopamine receptor blocking agent and by hypothalamic dopamine depleting drugs. We propose that dopamine regulates, either directly or indirectly, DNA synthesis in the lactotrophs of the pituitary gland, which may be responsive to negative feedback mechanisms.

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CLEBOPRIDE: A DOPAMINE RECEPTOR BLOCKING AGENT

InPharma ◽

10.1007/bf03300211 ◽

1982 ◽

Vol 330 (1) ◽

pp. 15-16

Keyword(s):

Dopamine Receptor ◽

Blocking Agent ◽

Receptor Blocking

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Paradoxical suppression of prolactin secretion: involvement of catecholaminergic mechanisms and the adrenal gland

Acta Endocrinologica ◽

10.1530/acta.0.1050463 ◽

1984 ◽

Vol 105 (4) ◽

pp. 463-467 ◽

Cited By ~ 3

Author(s):

Richard J. Krieg ◽

Steven W.J. Lamberts ◽

Robert M. MacLeod

Keyword(s):

Adrenal Gland ◽

Restraint Stress ◽

Blocking Agent ◽

Prolactin Secretion ◽

Female Rats ◽

Highly Sensitive ◽

The Central Nervous System ◽

Pre Treatment ◽

Plasma Prl ◽

Catecholaminergic Mechanisms

Abstract. Prolactin (Prl) secretion is normally elevated on the afternoon of pro-oestrus in the rat. Studies have shown that ether stress caused a 'paradoxical inhibiting effect' on these high Prl levels. The present study was designed to investigate whether the paradoxical suppression of Prl was mediated by the central nervous system or the adrenal glands. Plasma was obtained from adult female rats after sampling via intra-atrial catheters from 16.25–18.45 h on the afternoon of pro-oestrus. Restraint stress administered between 16.45–17.00 h induced the expected precipitous decrease in plasma Prl in intact animals. Pre-treatment of intact animals with the catecholamine receptor blocking agent haloperidol (1.0 mg/kg at 13.00 h) resulted in a further elevation of plasma Prl levels as compared with untreated controls, but eliminated the decrease of Prl in response to restraint stress. Although acutely adrenalectomized (ADX) animals proved to be highly sensitive to the bleeding procedures, initial Prl levels on the afternoon of pro-oestrus were not different from those of intact animals. Restraint stress under conditions of acute ADX was not found to induce the expected suppression of high Prl levels. Rather, the response was opposite to that which occurred in intact animals. These results indicate that the paradoxical suppression of Prl by restraint stress was mediated by catecholaminergic mechanisms, and that the adrenal gland was essential for the effect.

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