Effect of CCK-33 on Prolactin and Apomorphine-Induced Growth Hormone Secretion in Man

Nair, N.P.V.; S, Lal; Lizondo, E.; Eugenio, Henry; Guyda, H.

doi:10.1055/s-2007-1018721

Cited by 11 publications

(3 citation statements)

References 6 publications

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“…Receptors for CCK-8 and CCK-4 occur in brain (Saito, Sankaran, Goldfine and Williams 1980) so that it is possible that the effect of CCK-8 is mediated by fragments of the octapeptide. In previous work CCK-33 (Nair, Lal, Lizondo, Eugenio and Guyda 1983), which is degraded to smaller peptides including CCK-8, had no effect on Apo-induced GH secretion.…”

Section: Discussionmentioning

confidence: 74%

CCK-8 Antagonizes Apomorphine-Induced Growth Hormone Secretion in Normal Subjects

Nair¹,

Lal²,

Eugenio³

et al. 1986

Horm Metab Res

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Cholecystokinin octapeptide (CCK-8) (5 ug iv over 10 minutes) administered to normal men had no effect on basal growth hormone (GH) or prolactin secretion but significantly antagonized the GH response to the dopamine (DA) receptor agonist, apomorphine HCI (Apo) (0.5 mg sc), 30 (P less than 0.05) and 45 minutes (P less than 0.01) after Apo injection (n = 8). These results are compatible with an inhibitory effect of CCK-8 on certain DA mechanisms in the hypothalamic-pituitary axis. Whether CCK-8 affects DA function in other brain regions in man is unknown.

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Section: Discussionmentioning

confidence: 74%

CCK-8 Antagonizes Apomorphine-Induced Growth Hormone Secretion in Normal Subjects

Nair¹,

Lal²,

Eugenio³

et al. 1986

Horm Metab Res

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“…Studies in rats have shown that central administration of CCK stimulates PRL and GH release [25] and PRL release from rat pituitary7 cell cul tures [26]. In addition, Vijayan and McCann [27] proved the physiological role of CCK on PRL regulation by show ing a decline in PRL plasma concentration after adminis tration of the CCK receptor antagonist proglumide [27], However, a study exploring the role of CCK on PRL and GH plasma levels in humans failed to detect any effect of CCK-33 on basal or apomorphine-induced release of these hormones [28], A postprandial increase in plasma cortisol [31] and PRL [32] levels has been described in humans. It has been postulated that a GI hormone may be responsible for such an effect.…”

Section: Discussionmentioning

confidence: 99%

“…Because of these neuroanatomical obser vations, several investigators have explored the effect of CCK on the hypothalamic-pituitary-adrenal (HPA) axis function [11][12][13][14][15][16][17][18][19][20][21] and on AVP [22][23][24], prolactin (PRL) [25][26][27][28] and growth hormone (GH) [25,28] release. To our knowledge, however, the role, if any, of CCK-8 on the functional activity of the HPA axis has not been evaluated in humans.…”

Section: Introductionmentioning

confidence: 99%

Effects of Cholecystokinin Octapeptide on the Hypothalamic-Pituitary-Adrenal Axis Function and on Vasopressin, Prolactin and Growth Hormone Release in Humans

et al. 1993

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Cholecystokinin (CCK), a gastrointestinal (GI) hormone, is also present in structures of the central nervous system such as cortex, hippocampus, amygdala, olfactory tubercle and in regions involved in the regulation of the pituitary function. Although a number of studies have evaluated the effects of CCK on hypothalamic-pituitary-adrenal (HPA) axis function and on arginine vasopressin (AVP), prolactin (PRL) and growth hormone (GH) plasma levels in the laboratory animal, its role in humans has not been explored. Hence, we examined the effects of the exogenous administration of this GI hormone on corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), cortisol, AVP, PRL and GH plasma levels in humans. To accomplish this, graded doses (0, 50, 140 and 420 ng/kg) of sulfated CCK octapeptide (CCK-8), the full biologically active peptide, were infused intravenously to healthy men in 30 min. Blood samples were collected 30 min and immediately before the infusion was started (baseline) and 15, 30, 45, 60 and 90 min thereafter. CRH, ACTH, and AVP were extracted from plasma proteins using cartridges of SepPak C18. These hormones and cortisol were measured by radioimmunoassay whereas PRL and GH were measured by immunoradiometric assay. CCK-8 increased plasma ACTH and cortisol levels only at the dose of 420 ng/kg, whereas it had no detectable effect on plasma CRH levels. It increased also plasma AVP levels at the doses of 140 and 420 ng/kg. However, this effect reached the statistical significance only at the highest dose tested. CCK-8 stimulated PRL and GH release in a dose-dependent fashion. The lowest stimulatory dose was 140 ng/kg for both hormones. In conclusion, these results suggest that CCK is capable of stimulating HPA axis function, AVP, PRL and GH release in humans. Because these endocrine effects of CCK were detected at doses higher than that found able to mimic postprandial levels of this hormone, to produce Gl-related effects, and to modulate the release of GI hormones, we speculate that CCK, released by the GI tract, may not play a physiologic role in the regulation of the pituitary function in humans.

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Drug-Induced Changes in Prolactin Secretion

Hell

Wernze

1988

Medical Toxicology

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Prolactin secretion is affected by various diseases as well as by many drugs in humans and animals. While marked hyperprolactinaemia suggests the presence of a pituitary tumor, moderate changes may also occur in various endocrine or non-endocrine disorders. Drugs can interfere with prolactin regulation via complex mechanisms at the hypothalamus or at the pituitary site, but possible changes in prolactin metabolism are poorly understood as yet. This survey of the literature up to June 1986 covers the influence of various groups of drugs and agents on the plasma prolactin level under various conditions. It contains information that will facilitate evaluation of whether hyper- or hypoprolactinaemia may result from therapeutic intervention or must be related to an underlying disease. It is obvious that more subtle changes can be revealed by the use of dynamic tests either to stimulate or to suppress prolactin secretion.

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Effect of CCK-33 on Prolactin and Apomorphine-Induced Growth Hormone Secretion in Man

Cited by 11 publications

References 6 publications

CCK-8 Antagonizes Apomorphine-Induced Growth Hormone Secretion in Normal Subjects

CCK-8 Antagonizes Apomorphine-Induced Growth Hormone Secretion in Normal Subjects

Effects of Cholecystokinin Octapeptide on the Hypothalamic-Pituitary-Adrenal Axis Function and on Vasopressin, Prolactin and Growth Hormone Release in Humans

Drug-Induced Changes in Prolactin Secretion

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