Pulsatile Growth Hormone and Prolactin: Effects of (+) Butaclamol, a Dopamine Receptor Blocking Agent

Endocrinology ◽  
1977 ◽  
Vol 101 (4) ◽  
pp. 1298-1303 ◽  
Author(s):  
J. O. WILLOUGHBY ◽  
P. BRAZEAU ◽  
J. B. MARTIN
Keyword(s):  
Growth Hormone ◽  
Dopamine Receptor ◽  
Blocking Agent ◽  
Receptor Blocking

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

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.

Hyperprolactinaemia and DNA synthesis in the pituitary gland of the rat

1983 ◽  
Vol 97 (1) ◽  
pp. 65-74 ◽  
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.

EFFECT OF INSULIN INDUCED HYPOGLYCAEMIA ON THE BLOOD LEVELS OF CATECHOLAMINES, GLUCAGON, GROWTH HORMONE, CORTISOL, C-PEPTIDE AND PROINSULIN BEFORE AND DURING MEDICATION WITH THE CARDIOSELECTIVE BETA-RECEPTOR BLOCKING AGENT METOPROLOL IN MAN

1978 ◽  
Vol 87 (3) ◽  
pp. 659-667 ◽  
Author(s):  
Bernt Hökfelt ◽  
Bengt-Göran Hansson ◽  
Lise G. Heding ◽  
Karl Olof Nilsson
Keyword(s):  
Growth Hormone ◽  
Moderate Hypertension ◽  
Limit Of Detection ◽  
Plasma Catecholamines ◽  
Blocking Agent ◽  
Blood Levels ◽  
Exogenous Insulin ◽  
Maximal Dose ◽  
C Peptide ◽  
Receptor Blocking

ABSTRACT Studies were performed in 8 males with moderate hypertension to explore the influence of metoprolol on the sensitivity to insulin and on the response to hypoglycaemia with respect to plasma catecholamines, glucagon, growth hormone and cortisol. C-peptide and proinsulin were determined in some instances. All subjects were studied before treatment, after one month on placebo and after 3 months on metoprolol. The final maximal dose used was 50–150 mg three times daily. The sensitivity to insulin was the same during all three conditions studied. The response in catecholamines, glucagon, growth hormone and cortisol following insulin induced hypoglycaemia was similar during placebo as compared to no treatment. Adrenaline, growth hormone and cortisol showed a greater response to hypoglycaemia during metoprolol whereas no difference was seen with respect to noradrenaline and glucagon. The half-life of exogenous insulin was the same before and during metoprolol (7.6 min). Metoprolol caused no changes in the basal C-peptide levels. During the hypoglycaemic phase C-peptide showed a continuous gradual fall, which was similar before and during metoprolol. Proinsulin was below the lower limit of detection before and following the injection of insulin both without treatment and during metoprolol.

scholarly journals Preventing Broodiness in Turkey Hens with a Dopamine Receptor Blocking Agent

1980 ◽  
Vol 59 (5) ◽  
pp. 1126-1131 ◽  
Author(s):  
J.R. MILLAM ◽  
W.H. BURKE ◽  
M.E. El HALAWANI ◽  
L.A. OGREN
Keyword(s):  
Dopamine Receptor ◽  
Blocking Agent ◽  
Receptor Blocking

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

1977 ◽  
Vol 86 (2) ◽  
pp. 251-256 ◽  
Author(s):  
Giuseppe Delitala
Keyword(s):  
Dopamine Receptor ◽  
Mechanism Of Action ◽  
Normal Subjects ◽  
Blocking Agent ◽  
Mechanisms Of Action ◽  
Prolactin Release ◽  
Receptor Blocking ◽  
Pre Treatment ◽  
Plasma Prl

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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