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Metoclopramide increases vasopressin secretion.

G Norbiato, M Bevilacqua, E Chebat

The Journal of Clinical Endocrinology and Metabolism

|September 1, 1986

Summary

Metoclopramide (MCP) stimulates vasopressin secretion in humans, independent of its effects on dopamine or prolactin. This finding was observed in normal, dehydrated, and water-diuresing subjects, but not in patients with central diabetes insipidus.

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Area of Science:

Endocrinology
Nephrology
Pharmacology

Background:

Metoclopramide (MCP) is known to stimulate aldosterone secretion.
The potential influence of MCP on vasopressin secretion in humans was previously uninvestigated.

Purpose of the Study:

To investigate whether metoclopramide (MCP) influences vasopressin secretion in humans.
To determine if MCP's effect on vasopressin is linked to its antidopaminergic or prolactin-releasing properties.

Main Methods:

Administered metoclopramide (MCP) intravenously to healthy subjects and assessed plasma vasopressin levels.
Evaluated MCP's effect on vasopressin in dehydrated subjects and during water diuresis.
Compared MCP's effects with other antidopaminergic agents (sulpiride, haloperidol, domperidone) and TRH.

Related Experiment Videos

Studied MCP's impact in patients with severe central diabetes insipidus.

Main Results:

Intravenous MCP significantly increased plasma vasopressin levels in recumbent normal subjects.
No significant changes in plasma osmolality or hemodynamics were observed, ruling them out as causes for increased vasopressin.
Other antidopaminergic drugs and TRH did not affect vasopressin levels, suggesting MCP's action is specific.
MCP stimulated vasopressin release in dehydrated subjects and reduced free water excretion during water diuresis.
MCP had no effect on vasopressin secretion or water excretion in patients with central diabetes insipidus.

Conclusions:

Metoclopramide (MCP) stimulates the release of biologically active vasopressin in humans.
The vasopressin-releasing effect of MCP is not mediated through its antidopaminergic or prolactin-releasing actions.
MCP's action appears to be dependent on a functional hypothalamic-pituitary-adrenal axis, as evidenced by the lack of effect in central diabetes insipidus.