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Corticotrophin and vasopressin responses to metoclopramide in patients with hypothalamic amenorrhoea
Author(s) -
Seki K.,
Kato T.,
Sekiya S.
Publication year - 1997
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1046/j.1365-2265.1997.t01-22-1150928.x
Subject(s) - metoclopramide , medicine , endocrinology , vasopressin , dopaminergic , radioimmunoassay , dopamine antagonist , prolactin , haloperidol , hormone , dopamine , vomiting
OBJECTIVE A dopamine (DA) antagonist, metoclopramide, stimulates ACTH secretion in some women with hypothalamic amenorrhoea (HA) but not in normal women. Metoclopramide may stimulate ACTH secretion by decreasing dopaminergic inhibition of ACTH release. Furthermore, metoclopramide stimulates AVP secretion, and AVP is a stimulator of ACTH. Therefore, AVP may also be involved in the ACTH responses to metoclopramide. The relation between AVP and ACTH responses to metoclopramide were evaluated in normal women and women with HA to obtain more insight into the role of DA in the regulation of ACTH and AVP secretion. DESIGN ACTH, cortisol and AVP levels were measured before and after the administration of metoclopramide in 11 normal women during the early follicular phase and 12 women with HA. MEASUREMENTS ACTH was measured by immunoradiometric assay. AVP and cortisol were measured by radioimmunoassay. RESULTS The administration of metoclopramide significantly increased circulating levels of ACTH and cortisol in the women with HA, but not in the normal women. It increased AVP levels both in the normal women and in the women with HA. The incremental AVP response to metoclopramide was not significantly different between the two groups of women. CONCLUSION The effect of metoclopramide on AVP secretion may not be dependent on central dopaminergic activity, and the ACTH and cortisol responses to metoclopramide in the women with hypothalamic amenorrhoea are not accounted for by the augmented AVP response to metoclopramide.

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