Pituitary-adrenocortical response to metoclopramide in patients with acromegaly and prolactinoma: A clinical evaluation of catecholamine-mediated adrenocorticotropin secretion

Seikoh Nishida, Michihiro Matsuki, Noriko Adachi, Masaharu Horino, Masaya Yoneda, Masahiko Endoh, Hideki Oyama, Masahisa Kikuoka, Ryoichi Otsuka, Ryoji Ishii, Chiyo Andoh

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

We have demonstrated that metoclopramide stimulates cortisol secretion at least in part by a stress-mediated effect in normal men. To examine further the effect of the drug on the hypothalamo-pituitary adrenal system, we studied the cortisol response to 20 mg metoclopramide in patients with acromegaly, prolactinomas, and functional hyperprolactinemia and compared the results with the responses to insulin-induced hypoglycemia. In some patients, the effects of metoclopramide on CRH-induced ACTH and cortisol increase were studied to determine whether a change in dopaminergic (catecholaminergic) activity altered CRH stimulation of pituitary-adrenal function. No cortisol response to 20 mg metoclopramide occurred in 13 tests on 8 of 9 patients with prolactinoma or acromegaly with hyperprolactinemia, whereas both acromegalic patients without hyperprolactinemia had a response. All of the patients had a normal cortisol response to insulin-induced hypoglycemia. Pretreatment with metoclopramide enhanced the CRH-induced cortisol increase from 30–120 min after CRH in normal men, but only at 15 and 30 min in 5 agromegalic patients. The results suggest that metoclopramide acts in the hypothalamus to release ACTH through a dopamine antagonist-mediated (catecholaminergic) mechanism, and that metoclopramide may act additively with CRH to stimulate ACTH secretion in normal men. The absence of a metoclopramide-induced cortisol response in patients with acromegaly or prolactinomas and the absence of a normal cortisol response to metoclopramide-CRH in acromegalic patients could be due to endogenous catecholamine deficiency in these patients.

Original languageEnglish
Pages (from-to)995-1001
Number of pages7
JournalJournal of Clinical Endocrinology and Metabolism
Volume64
Issue number5
DOIs
Publication statusPublished - 1987
Externally publishedYes

Fingerprint

Prolactinoma
Metoclopramide
Acromegaly
Adrenocorticotropic Hormone
Catecholamines
Hydrocortisone
Hyperprolactinemia
Hypoglycemia
Pituitary-Adrenal System
Insulin
Dopamine Antagonists
Hypothalamus

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Biochemistry
  • Endocrinology
  • Clinical Biochemistry
  • Biochemistry, medical

Cite this

Pituitary-adrenocortical response to metoclopramide in patients with acromegaly and prolactinoma : A clinical evaluation of catecholamine-mediated adrenocorticotropin secretion. / Nishida, Seikoh; Matsuki, Michihiro; Adachi, Noriko; Horino, Masaharu; Yoneda, Masaya; Endoh, Masahiko; Oyama, Hideki; Kikuoka, Masahisa; Otsuka, Ryoichi; Ishii, Ryoji; Andoh, Chiyo.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 64, No. 5, 1987, p. 995-1001.

Research output: Contribution to journalArticle

Nishida, Seikoh ; Matsuki, Michihiro ; Adachi, Noriko ; Horino, Masaharu ; Yoneda, Masaya ; Endoh, Masahiko ; Oyama, Hideki ; Kikuoka, Masahisa ; Otsuka, Ryoichi ; Ishii, Ryoji ; Andoh, Chiyo. / Pituitary-adrenocortical response to metoclopramide in patients with acromegaly and prolactinoma : A clinical evaluation of catecholamine-mediated adrenocorticotropin secretion. In: Journal of Clinical Endocrinology and Metabolism. 1987 ; Vol. 64, No. 5. pp. 995-1001.
@article{d8dc97021fcb44b8a19301bf60769d30,
title = "Pituitary-adrenocortical response to metoclopramide in patients with acromegaly and prolactinoma: A clinical evaluation of catecholamine-mediated adrenocorticotropin secretion",
abstract = "We have demonstrated that metoclopramide stimulates cortisol secretion at least in part by a stress-mediated effect in normal men. To examine further the effect of the drug on the hypothalamo-pituitary adrenal system, we studied the cortisol response to 20 mg metoclopramide in patients with acromegaly, prolactinomas, and functional hyperprolactinemia and compared the results with the responses to insulin-induced hypoglycemia. In some patients, the effects of metoclopramide on CRH-induced ACTH and cortisol increase were studied to determine whether a change in dopaminergic (catecholaminergic) activity altered CRH stimulation of pituitary-adrenal function. No cortisol response to 20 mg metoclopramide occurred in 13 tests on 8 of 9 patients with prolactinoma or acromegaly with hyperprolactinemia, whereas both acromegalic patients without hyperprolactinemia had a response. All of the patients had a normal cortisol response to insulin-induced hypoglycemia. Pretreatment with metoclopramide enhanced the CRH-induced cortisol increase from 30–120 min after CRH in normal men, but only at 15 and 30 min in 5 agromegalic patients. The results suggest that metoclopramide acts in the hypothalamus to release ACTH through a dopamine antagonist-mediated (catecholaminergic) mechanism, and that metoclopramide may act additively with CRH to stimulate ACTH secretion in normal men. The absence of a metoclopramide-induced cortisol response in patients with acromegaly or prolactinomas and the absence of a normal cortisol response to metoclopramide-CRH in acromegalic patients could be due to endogenous catecholamine deficiency in these patients.",
author = "Seikoh Nishida and Michihiro Matsuki and Noriko Adachi and Masaharu Horino and Masaya Yoneda and Masahiko Endoh and Hideki Oyama and Masahisa Kikuoka and Ryoichi Otsuka and Ryoji Ishii and Chiyo Andoh",
year = "1987",
doi = "10.1210/jcem-64-5-995",
language = "English",
volume = "64",
pages = "995--1001",
journal = "Journal of Clinical Endocrinology and Metabolism",
issn = "0021-972X",
publisher = "The Endocrine Society",
number = "5",

}

TY - JOUR

T1 - Pituitary-adrenocortical response to metoclopramide in patients with acromegaly and prolactinoma

T2 - A clinical evaluation of catecholamine-mediated adrenocorticotropin secretion

AU - Nishida, Seikoh

AU - Matsuki, Michihiro

AU - Adachi, Noriko

AU - Horino, Masaharu

AU - Yoneda, Masaya

AU - Endoh, Masahiko

AU - Oyama, Hideki

AU - Kikuoka, Masahisa

AU - Otsuka, Ryoichi

AU - Ishii, Ryoji

AU - Andoh, Chiyo

PY - 1987

Y1 - 1987

N2 - We have demonstrated that metoclopramide stimulates cortisol secretion at least in part by a stress-mediated effect in normal men. To examine further the effect of the drug on the hypothalamo-pituitary adrenal system, we studied the cortisol response to 20 mg metoclopramide in patients with acromegaly, prolactinomas, and functional hyperprolactinemia and compared the results with the responses to insulin-induced hypoglycemia. In some patients, the effects of metoclopramide on CRH-induced ACTH and cortisol increase were studied to determine whether a change in dopaminergic (catecholaminergic) activity altered CRH stimulation of pituitary-adrenal function. No cortisol response to 20 mg metoclopramide occurred in 13 tests on 8 of 9 patients with prolactinoma or acromegaly with hyperprolactinemia, whereas both acromegalic patients without hyperprolactinemia had a response. All of the patients had a normal cortisol response to insulin-induced hypoglycemia. Pretreatment with metoclopramide enhanced the CRH-induced cortisol increase from 30–120 min after CRH in normal men, but only at 15 and 30 min in 5 agromegalic patients. The results suggest that metoclopramide acts in the hypothalamus to release ACTH through a dopamine antagonist-mediated (catecholaminergic) mechanism, and that metoclopramide may act additively with CRH to stimulate ACTH secretion in normal men. The absence of a metoclopramide-induced cortisol response in patients with acromegaly or prolactinomas and the absence of a normal cortisol response to metoclopramide-CRH in acromegalic patients could be due to endogenous catecholamine deficiency in these patients.

AB - We have demonstrated that metoclopramide stimulates cortisol secretion at least in part by a stress-mediated effect in normal men. To examine further the effect of the drug on the hypothalamo-pituitary adrenal system, we studied the cortisol response to 20 mg metoclopramide in patients with acromegaly, prolactinomas, and functional hyperprolactinemia and compared the results with the responses to insulin-induced hypoglycemia. In some patients, the effects of metoclopramide on CRH-induced ACTH and cortisol increase were studied to determine whether a change in dopaminergic (catecholaminergic) activity altered CRH stimulation of pituitary-adrenal function. No cortisol response to 20 mg metoclopramide occurred in 13 tests on 8 of 9 patients with prolactinoma or acromegaly with hyperprolactinemia, whereas both acromegalic patients without hyperprolactinemia had a response. All of the patients had a normal cortisol response to insulin-induced hypoglycemia. Pretreatment with metoclopramide enhanced the CRH-induced cortisol increase from 30–120 min after CRH in normal men, but only at 15 and 30 min in 5 agromegalic patients. The results suggest that metoclopramide acts in the hypothalamus to release ACTH through a dopamine antagonist-mediated (catecholaminergic) mechanism, and that metoclopramide may act additively with CRH to stimulate ACTH secretion in normal men. The absence of a metoclopramide-induced cortisol response in patients with acromegaly or prolactinomas and the absence of a normal cortisol response to metoclopramide-CRH in acromegalic patients could be due to endogenous catecholamine deficiency in these patients.

UR - http://www.scopus.com/inward/record.url?scp=0023194946&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0023194946&partnerID=8YFLogxK

U2 - 10.1210/jcem-64-5-995

DO - 10.1210/jcem-64-5-995

M3 - Article

C2 - 3031125

AN - SCOPUS:0023194946

VL - 64

SP - 995

EP - 1001

JO - Journal of Clinical Endocrinology and Metabolism

JF - Journal of Clinical Endocrinology and Metabolism

SN - 0021-972X

IS - 5

ER -