Effect of Metoclopramide on Serum Prolactin Levels in Humans

Delitala, G.; Masala, A.; Devilla, L.

doi:10.1111/j.1365-2265.1976.tb03877.x

Cited by 37 publications

(20 citation statements)

References 8 publications

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“…It is now established that metoclopramide is a potent stimulus to prolactin secretion (Delitala et al, 1976;Judd et al, 1976;McCallum et al, 1976), and indeed not only is the magnitude of prolactin response greater than that seen after TRH, but it is also more prolonged in duration. In response to both TRH and metocIopramide stimulation, prolactin release is considerably greater in women, a finding that may reflect greater oestrogen-related prolactin reserve despite remarkably similar basal levels in men and women.…”

Section: Discussionmentioning

confidence: 99%

Laboratory Assessment of Prolactin Status

et al. 1979

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SUMMARYThe laboratory assessment of prolactin status was evaluated by detailed study of 921 subjects (587 normal subjects and 334 patients with pathological conditions). The effect on serum prolactin levels of age, sex, circadian rhythm, pulsatility of secretion, stress, drug ingestion, and pregnancy was defined in normal subjects. The normal prolactin responses to stimulation (TRH, metoclopramide) and suppression (t-dopa, bromocriptine) were also determined. Basal prolactin levels were measured in patients with defined pathological conditions including prolactinoma, idiopathic hyperprolactinaemia, acromegaly, Cushing's disease, chronic renal failure, primary hypothyroidism, pituitary ablation, Kallman's syndrome, Nelson's syndrome, growth hormone deficiency, gonadotrophin deficiency, craniopharyngioma, panhypopituitarism, and chronic progressive arthropathy. Based on these data, a strategy for the routine laboratory assessment of prolactin status is outlined. NORMAL SUBJECTS

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Section: Discussionmentioning

confidence: 99%

Laboratory Assessment of Prolactin Status

et al. 1979

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“…Metoclopramide is effective in blocking dopamine receptors in the central nervous system (20), gut (21), and cardiovascular system (22). It also is a potent stimulator of prolactin release in vivo (23,24) and acts in vitro to antagonize the inhibitory effect of dopamine on prolactin release (17).…”

Section: Discussionmentioning

confidence: 99%

Effects of Metoclopramide and Bromocriptine on the Renin-Angiotensin-Aldosterone System in Man

Carey¹,

Thorner²,

Ortt³

1979

J. Clin. Invest.

231

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A B S T R A C T This study was designed to investigate the possible role of dopaminergic mechanisms in the control ofthe renin-angiotensin-aldosterone system in normal man. Six normal male subjects in metabolic balance at 150 meq sodium, 60 meq potassium constant intake received the specific dopamine antagonist, metoclopramide, 10 mg i.v. or placebo followed by angiotensin II infusion 1 h later on 2 consecutive days. Metoclopramide increased plasma aldosterone concentration from 8.2+2.2 to 21.0+3.3 ng/100 ml (P <0.005) and plasma prolactin concentration from 18.0±4.0 to 91.7+4.0 nglml (P < 0.001) within 15 min of its administration. At 1 h, plasma aldosterone and prolactin concentrationis remained elevated at 16.8 ±2.1 ng/100 ml (P < 0.01) and 86.8±+15.9 ng/ml (P < 0.005), respectively. Angiotensin II at 2, 4, and 6 pmol/kg per miim further increased plasma aldosterone concentration to 27.2+3.4, 31.9+5.7, and 36.0+6.7 ng/100 ml (P < 0.02), respectively. Placebo did not alter plasma aldosterone or prolactin concentrations, but angiotensin II increased plasma aldosterone concentration to 13.7±2.4, 19.0+ 1.9, and 23.3+3.2 ngIl00 ml (P < 0.005). The increment of plasma aldosterone concentration in response to angiotensin II was similar after metoclopramide or placebo.The six subjects also received the dopamine agonist, bromocriptine, 2.5 mg or placebo at 6 p.m., midnight, and 6 a.m. followed by angiotensin II infusion on 2 consecutive d. Bromocriptine suppressed prolactin to <3 ng/ml. After placebo, plasma aldosterone concentration increased from 5.2± 1.4 to 12.3+1.7, 17.2 +2.2, and 21.8+3.5 ng/100 ml (P < 0.01) and after bromocriptine from 7.2±1.0 to 14.7+. and 23.4±1.6 ng/100 ml (P < 0.001) with each respective angiotensin II dose. No difference in the response to angiotensin II after bromocriptine or placebo was observed. Plasma renin activity, free 11-hydroxycorticoid concentration, and serum potassium concentration were unchanged by metoclopramide or bromocriptine.The results suggest that aldosterone production is under maximum tonic dopaminergic inhibition which can be overridden with stimulation by angiotensin II in normal man. INTRODUCTION Dopamine, a precursor of the sympathetic neurotransmitter norepinephrine, may itself be a major transmitter of the peripheral autonomic nervous system (1). The adrenergic component of this system is important in controlling renin release (2, 3), but little is known concerning the role of dopamine in the regulation of the renin-angiotensin-aldosterone system. Cuche et al. (4) have shown in man that the increase in plasma renin activity with upright posture is associated with a decrease in urinary dopamine and an increase in norepinephrine and epinephrine excretion. Alexander and colleagues (5) have reported that sodium-depleted subjects respond to dietary or intravenous sodium loading with an increase in urinary dopamine and a decrease in urinary norepinephrine. Thus, maneuvers which would be expected to alter the activity of the renin-angiotensin-aldosterone system are ass...

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“…Single acute doses of metoclopramide increase serum prolactin levels for as long as 9 h (2) and administration of metoclopramide for 1 week results in increased serum prolactin concentrations (3,4). Although long-term therapy with metoclopramide has been associated with galactorrhea (5), serum prolactin measurements were not reported in these patients.…”

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confidence: 96%

Effect of Chronic Metoclopramide Therapy on Serum Pituitary Hormone Concentrations

Tamagna¹,

Lane²,

Hershman³

et al. 1979

Horm Res

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The effect of chronic (3-9 months) therapy with metoclopramide on serum levels of pituitary and thyroid hormones was studied in 4 males and 1 female. The mean serum prolactin concentration during metoclopramide therapy was significantly higher than after discontinuation of metoclopramide. Serum prolactin concentrations increased acutely after each dose of metoclopramide, and gradually returned to normal by 6-12 h. There were no significant differences in the serum TSH, T₃, T₄, GH, and gonadotrophin levels during and after metoclopramide administration. In the male subjects the mean serum testosterone was normal, but significantly lower during metoclopramide therapy.

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Effect of Metoclopramide on Serum Prolactin Levels in Humans

Cited by 37 publications

References 8 publications

Laboratory Assessment of Prolactin Status

Laboratory Assessment of Prolactin Status

Effects of Metoclopramide and Bromocriptine on the Renin-Angiotensin-Aldosterone System in Man

Effect of Chronic Metoclopramide Therapy on Serum Pituitary Hormone Concentrations

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