Effects of Acute and Chronic Administration of Narcotic Analgesics on Growth Hormone and Corticotrophin (ACTH) Secretion in Rats

Kokka, Norio; Garcia, Joseph F.; Elliott, Henry W.

doi:10.1016/s0079-6123(08)64091-1

Cited by 68 publications

(24 citation statements)

References 9 publications

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“…1). Morphine, which is known to be a strong stimulus for ACTH secretion (12,15), also significantly increased plasma ir-f3-endorphin in our experiments (Fig. 2).…”

Section: Resultssupporting

confidence: 68%

“…Effects of stress, dexamethasone pretreatment, or both treatments on PRL and ir-,B-endorphin blood levels were evaluated in four groups of five rats pretreated with dexamethasone or saline as above. At time 0, animals were subjected to inescapable electric footshocks; blood samples were taken after 15 Subjects for all the experiments were 200-g male SpragueDawley rats (Simonson Farms, Gilroy, CA).…”

Section: Methodsmentioning

confidence: 99%

“…Secretion was provoked by stress or morphine after animals were pretreated with naloxone or dexamethasone. The latter, a potent synthetic glucocorticoid, is known to suppress the morphine and stress-induced release of ACTH (14,15).…”

mentioning

confidence: 99%

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Stress-induced release of prolactin: blockade by dexamethasone and naloxone may indicate beta-endorphin mediation.

Rossier¹,

French²,

Rivier³

et al. 1980

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

108

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Basal levels of immunoreactive (ir) 4-endorphin, corticotropin (ACTH), and prolactin (PRL) in plasma of male rats decrease after dexamethasone pretreatment (400 ,sg/kg at 24 hr and 200 sg/kg at 2 hr before). Inescapable electric footshocks increase ir-p-endorphin, ACTH, and PRL plasma levels, and this effect is blocked by dexamethasone pretreatment. Morphine (20 mg/kg) also increases ir-O-endo in, ACTH, and PRL levels. Dexamethasone pretreatment blocks the morphine-induced release of ir-p-endorphin but does not prevent the morphine-induced release of PRL. Naloxone, the opiate antagonist, decreases basal plasma levels of PRL and partially blocks the stress-induced increase of PRL, but it has no effect on the basal or stress-induced release of ir--endorphin.These results are consistent with the proposal that P-endorphin may interact with an opiate receptor involved in the regulation of PRL secretion.Since the early studies by Selye (1), corticotropin (ACTH) has been recognized as the primary pituitary hormone secreted in response to acute stress in all species studied. Nicoll et al. (2) recognized that prolactin (PRL) was also released by stress.Recently, we reported that immunoreactive (ir) f3-endorphin was secreted in response to stress (3,4). Moreover, we showed that ir-f3-endorphin and ACTH were secreted concomitantly in nearly equimolar amounts.3-Lipotropin, the pituitary hormone of which f,-endorphin is amino acid sequence 61-91, was reported earlier to be released by stress (5). Although one recent report claimed that apparent f3-endorphin immunoreactivity in human blood was due only to the crossreactivity of the antiserum with f3-lipotropin (6), more recent reports from different laboratories have shown that, in fact, a 3-endorphin-like substance does exist in human and rat blood and that its levels are higher after stress (7-11). Nevertheless, the role of f3-endorphin in peripheral blood is still under scrutiny.In this study, we examined the possibility that f3-endorphin released by stress into the blood could promote the secretion of another pituitary hormone, PRL In order to test the possibility that f3-endorphin released by stress promotes PRL secretion through an opiate receptor, we compared the secretion of PRL and of fl-endorphin. Secretion was provoked by stress or morphine after animals were pretreated with naloxone or dexamethasone. The latter, a potent synthetic glucocorticoid, is known to suppress the morphine and stress-induced release of ACTH (14, 15). MATERIALS AND METHODSDesign of Experiments and Statistical Evaluation. The effects of dexamethasone pretreatment on footshock-induced release of ,3-endorphin were studied by using a two-way repeated measures design. In nine rats, a catheter (Corning Silastic) was implanted in the right jugular vein, passed under the skin, and mounted to a Luer needle hub on the skull by stainless steel screws and dental cement. This method allowed blood sampling during experimental manipulations without undue stress to the rats. Patency of catheters was...

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“…1). Morphine, which is known to be a strong stimulus for ACTH secretion (12,15), also significantly increased plasma ir-f3-endorphin in our experiments (Fig. 2).…”

Section: Resultssupporting

confidence: 68%

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Stress-induced release of prolactin: blockade by dexamethasone and naloxone may indicate beta-endorphin mediation.

Rossier¹,

French²,

Rivier³

et al. 1980

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

108

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“…In addition the basal and stress-induced secretion of 'Author for correspondence. corticosterone in the rat have been shown by a number of laboratories to be modulated by the acute administration of opioid agonists (Kokka et al, 1973;Eisenberg, 1985;Pechnick et al, 1985a) and opioid antagonists (Eisenberg, 1980;Siegel et al, 1982;Jezova et al, 1982).…”

Section: Introductionmentioning

confidence: 99%

Developmental responses to opioids reveals a lack of effect on stress‐induced corticosterone levels in neonatal rats

Bailey

Kitchen

1987

British J Pharmacology

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1 The neonate has an unusual capacity for survival and the possibility exists that mechanisms for controlling stress responses may differ in the developing animal. In adults both endogenous and exogenous opioids can modulate the corticosterone responses to stress. We have studied this effect in neonatal rats and found that opioid modulation is absent in early postnatal development.2 Neonatal rats ofeither sex were injected with morphine (5-50mg kg-'), fentanyl (10-100 .tLg kg-'), buprenorphine (O.1-30 mg kg') or naloxone (O.1-Omg kg-') and plasma corticosterone measured fluorimetrically 15 or 20 min later. In addition naloxone reversibility studies (1 mg kg-', co-administered) were carried out for the opioid agonists. 3 In adult rats, elevations in plasma corticosterone caused by injection stress were potentiated by morphine, fentanyl and buprenorphine. In neonates, though injection stress-induced rises in plasma corticosterone were absent at 10 days, elevations were observed at 21 days and later. However, significant potentiation of this corticosterone response by fentanyl was absent at 21 days and at later ages (30 and 40 days) for morphine and buprenorphine. The potentiating effect of all three agonists did not become fully effective until day 45. In addition, in animals acclimatized to injection stress by 7 day injection pretreatment, fentanyl did not significantly alter corticosterone levels in 30 day old neonates.4 High doses ofnaloxone (10mg kg-')significantly increased the corticosterone response to injection stress in adult rats but this effect was absent in 30 day old animals. A dose of naloxone (I mg kg-') which had no significant effect on the corticosterone response inhibited the effects of morphine, fentanyl and buprenorphine in 45 day old and adult rats. 5 This late development of opioid action is unusual in comparison with the maturation of endogenous peptides, receptors and antinociceptive responses and suggests that alternative mechanisms may be involved in stress-control in the neonate.

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“…Kokka et al (5) and Suzuki et al (10) demonstrated that the rise of plasma cor ticosterone level by morphine was an tagonized by naloxone. ACTH or formalin also increased plasma corticosterone level dose-dependently (3).…”

mentioning

confidence: 98%

Participation of the Nucleus Reticularis Gigantocellularis in the Morphine-Induced Elevation of Plasma Corticosterone in Rats

Kishioka¹,

Tamura²,

Iguchi³

et al. 1985

Japanese Journal of Pharmacology

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Abstract-The effects of morphine, adrenocorticotropic hormone (ACTH) and formalin on plasma corticosterone levels were investigated in the nucleus reticularis gigantocellularis (NRGC)-lesioned rats. ACTH (1.0 U/kg) or formalin (6.4%, 0.2 ml/rat) elevated plasma corticosterone in both sham-lesioned and NRGC-lesioned rats at the same degree, while morphine (10 mg/kg) also elevated plasma corticos terone in sham-lesioned rats, the elevation of which was significantly reduced by NRGC-lesioning.These findings suggest that the NRGC is involved in the cor ticosterone-increasing effect of morphine, but not involved in the effect of ACTH or formalin.

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Effects of Acute and Chronic Administration of Narcotic Analgesics on Growth Hormone and Corticotrophin (ACTH) Secretion in Rats

Cited by 68 publications

References 9 publications

Stress-induced release of prolactin: blockade by dexamethasone and naloxone may indicate beta-endorphin mediation.

Stress-induced release of prolactin: blockade by dexamethasone and naloxone may indicate beta-endorphin mediation.

Developmental responses to opioids reveals a lack of effect on stress‐induced corticosterone levels in neonatal rats

Participation of the Nucleus Reticularis Gigantocellularis in the Morphine-Induced Elevation of Plasma Corticosterone in Rats

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