Beta-endorphin: stimulation of growth hormone release in vivo.

Dupont, André; Cusan, Lionel; Garon, Marie; Labrie, Fernand; Li, Choh Hao

doi:10.1073/pnas.74.1.358

Cited by 105 publications

(24 citation statements)

References 17 publications

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“…The rapid rise in plasma prolactin after iv 1h-ep without any increase in plasma growth hormone is similar to the effect of iv morphine in humans (20); this finding contrasts with the effect of /3h-ep in rats, in which stimulation of both growth hormone and prolactin secretion has been reported (21,22). It has previously been reported that morphine stimulation of growth hormone secretion in the rat is a dose-related phenomenon and does not occur at doses of 50 jug/kg or less (23); similar dose-related effects in rats have been shown with 1h-ep (21,22). Nevertheless, with the icv doses of 3h-ep that we have administered, there was decreased plasma growth hormone secretion in the presence of increased plasma prolactin.…”

Section: Methodscontrasting

confidence: 51%

β-Endorphin: Analgesic and hormonal effects in humans

Foley

Kourides

Inturrisi

et al. 1979

Proc. Natl. Acad. Sci. U.S.A.

171

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The pharmacokinetics and the hormonal, analgesic, and behavioral effects of several doses of human a-endorphin were evaluated after intravenous administration to three patients and intracerebroventricular administration to one patient with pain caused by cancer. These effects were compared to the hormonal effects of intravenously administered morphine sulfate in two patients and an enkephalin analog in two baboons. The mean terminal half-life after intravenous administration of 5 or 10 mg of human f-endorphin to three patients was 37 min; the mean volume of distribution was 178 ml/kg, and the metabolic clearance rate was 3.2 (ml/min)/kg.The half-life of P-endorphin in cerebrospinal fluid after intracerebroventricular administration was 93 min, and the volume of distribution was 0.74 ml/kg. A rapid rise in plasma prolactin followed both intravenous and intracerebroventricular a-endorphin. Intravenous administration did not affect plasma growth hormone, but intracerebroventricular administration suppressed plasma growth hormone. No significant change in plasma growth hormone was noted after intravenous administration of morphine to humans, but plasma growth hormone decreased in one baboon after administration of the enkephalin analog. P-Endorphin-stimulated release of prolactin occurred at doses lower than those required to produce analgesic and other behavioral effects. When both hormonal and analgesic effects were observed (after 7.5 mg were given intracerebroventricularly), the onset of the hormonal response slightly preceded the analgesic and behavioral responses. These studies suggest that the hormonal effects of ,-endorphin are species dependent and are similar to those of morphine. Hormonal and analgesic effects of ,-endorphin appear to result from the activation of opiate receptors that differ in their locations and characteristics.Intracerebroventricular (icv) administration of f3-endorphin causes similar physiological and pharmacological effects in several animal species (1, 2). In contrast, intravenous (iv) administration of ,B-endorphin causes different effects in different species. In the rat there is no demonstrable behavioral effect after iv doses of f3-endorphin up to 30 mg/kg (3), whereas in the cat doses as low as 50-500 jug/kg produce behavioral changes (4). Preliminary studies in humans (5-7), using a wide dose range of human fl-endorphin (f.h-ep), revealed both behavioral and analgesic effects. In the present study, we have assessed the pharmacologic disposition, as well as the concurrent hormonal, analgesic, and behavioral effects of Oh-ep administered in various doses iv to three cancer patients with pain and icv to one other cancer patient with pain. We administered an enkephalin analog, [2-D-alanine,5-norleucinelenkephalinamide, to two baboons to evaluate whether the hormonal and behavioral effects of opioid peptides were similar in nonhuman primates without pain or previous exposure to opiate drugs. 100 ,ug to 7.5 mg at 1-2 week intervals over a 10-week period; the reservoir had...

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Section: Methodscontrasting

confidence: 51%

β-Endorphin: Analgesic and hormonal effects in humans

Foley

Kourides

Inturrisi

et al. 1979

Proc. Natl. Acad. Sci. U.S.A.

171

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“…Although it has been recently shown that opioid peptides elevate the circulating levels of GH and PRL in man and in experimental animals (46)(47)(48)(49)(50), there is a controversy regarding the mechanism ofaction ofopioid peptides to stimulate hormone release. In rat pituitaries, opioid peptides were found to counteract the inhibitory effect of dopamine on PRL secretion in vitro (51).…”

Section: Methodsmentioning

confidence: 99%

Direct effects of catecholamines, thyrotropin-releasing hormone, and somatostatin on growth hormone and prolactin secretion from adenomatous and nonadenomatous human pituitary cells in culture.

Ishibashi¹,

Yamaji²

1984

J. Clin. Invest.

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A bstract. To determine the mechanism and the site of action of catecholamines as well as hormones including thyrotropin-releasing hormone (TRH)' and somatostatin on pituitary hormone release in patients with acromegaly and in normal subjects, the effects of these substances on growth hormone (GH) and prolactin (PRL) secretion from adenomatous and nonadenomatous human pituitary cells in culture were examined. When dopamine (0.01-0.1 tM) or bromocriptine (0.01-0.1 tM) was added to the culture media, a significant inhibition of GH

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“…Furthermore, the synthetic enkephalin analogue, FK-33-824, causes GH release in man (39). None of the opioids appear to act directly at the pituitary level, and it is likely that they influence the release of GH either by modulating the secretion of releasing-inhibiting factors and/or by affecting neurotransmitters (40,41). Evidence supporting the latter hypothesis was provided in a recent study demonstrating that a-adrenergic receptor blockade with phenoxybenzamine or inhibition of NE and EPI synthesis with diethyldithiocarbamate, a dopamine-13-hydroxylase inhibitor, abolished the GH-releasing effect of morphine in the rat (17).…”

Section: Effectsmentioning

confidence: 99%

Regulation of Episodic Growth Hormone Secretion by the Central Epinephrine System

Terry

Crowley

Johnson³

1982

J. Clin. Invest.

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A B S T R A C T Catecholamines are postulated to regulate growth hormone (GH) secretion by their influence on the release of two hypothalamic substances, somatostatin, which inhibits GH release, and GH-releasing factor, as yet unidentified. Extensive pharmacologic studies in man and animals indicate a stimulatory effect of central norepinephrine and dopamine on GH, but the function of epiphephrine (EPI) is uncertain. Furthermore, many of the agents used to study the role of catecholamines in GH regulation are not selective in that they affect adrenergic as well as noradrenergic and/or dopaminergic neurotransmission. In the present investigation, central nervous system (CNS) EPI

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Beta-endorphin: stimulation of growth hormone release in vivo.

Cited by 105 publications

References 17 publications

β-Endorphin: Analgesic and hormonal effects in humans

β-Endorphin: Analgesic and hormonal effects in humans

Direct effects of catecholamines, thyrotropin-releasing hormone, and somatostatin on growth hormone and prolactin secretion from adenomatous and nonadenomatous human pituitary cells in culture.

Regulation of Episodic Growth Hormone Secretion by the Central Epinephrine System

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