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  • 1
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    Naloxone inhibits and morphine potentiates the adrenal steroidogenic response to ACTH (1981)
    In:  Other Sources
    Details
    Publication Date: 2011-08-24
    Description: The administration of morphine to hypophysectomized rats potentiated the steroidogenic response of the adrenal cortex to exogenous adrenocorticotrophic hormone (ACTH) in a dose-dependent fashion. Conversely, the opiate antagonist naloxone inhibited the adrenal response to ACTH. Naloxone pretreatment also antagonized the potentiating effect of morphine on ACTH-induced steroidogenesis in a dose-dependent manner. Neither morphine nor naloxone, administered to hypophysectomized rats, had any direct effect on adrenal steroidogenesis. These adrenal actions were stereospecific since neither the (+)-stereoisomer of morphine, nor that or naloxone, had any effect on the adrenal response to ACTH. The administration of human beta-endorphin to hypophysectomized rats had no effect on the adrenal corticosterone concentration nor did it alter the response of the adrenal gland to ACTH. These results indicate that morphine can potentiate the action of ACTH on the adrenal by a direct, stereospecific, dose-dependent mechanism that is prevented by naloxone pretreatment and which may involve competition for ACTH receptors on the corticosterone-secreting cells of the adrenal cortex.
    Keywords: Life Sciences (General)
    Type: European journal of pharmacology (ISSN 0014-2999); Volume 75; 1; 1-6
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  • 2
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    Inhibition of the pituitary-adrenal response to stress during deprivation-induced feeding (1979)
    In:  Other Sources
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    Publication Date: 2011-08-17
    Description: Plasma corticosterone and plasma and pituitary ACTH concentrations were determined during feeding and after application of an acute stress at various times after food and water presentation to male rats maintained on a restricted feeding and watering schedule. Both plasma corticosterone and ACTH concentrations fell after the presentation of food and water, and this fall was accompanied by increased levels of ACTH in the pituitary gland. In addition, a rise in plasma levels of ACTH was inhibited in response to an acute stress applied at 0-5 min after presentation of food and water, but ACTH synthesis was not. This inhibition of ACTH and corticosterone secretion in response to stress was transient and dissipated as a relatively linear function of the interval between food presentation and application of the stress. The results suggest that this feeding-induced, corticosteroid-independent inhibition of pituitary-adrenal activity involves active inhibitory mechanisms operating initially on ACTH secretory processes of the pituitary and later on the synthesis of ACTH or on the secretion of hypothalamic corticotropin-releasing factor.
    Keywords: LIFE SCIENCES (GENERAL)
    Type: Endocrinology; 104; 4, 19; 1979
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  • 3
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    Synaptosomal uptake of hypothalamic monoamines and recovery of pituitary-adrenal activity following medial forebrain bundle lesions in rats (1979)
    In:  Other Sources
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    Publication Date: 2011-08-17
    Keywords: LIFE SCIENCES (GENERAL)
    Type: Neuroendocrinology; 28; 1979
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  • 4
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    Effects of fenfluramine administration on activity of the pituitary-adrenal system in the rat (1978)
    In:  Other Sources
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    Publication Date: 2011-08-17
    Keywords: LIFE SCIENCES (GENERAL)
    Type: Western Pharmacology Society; vol. 21
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  • 5
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    ACTH-like peptides increase pain sensitivity and antagonize opiate analgesia (1981)
    In:  CASI
    Details
    Publication Date: 2019-06-28
    Description: The role of the pituitary and of ACTH in pain sensitivity was investigated in the rat. Pain sensitivity was assessed by measuring paw-lick and jump latencies in response to being placed on a grid at 55 C. Hypophysectomy reduced pain sensitivity, and this effect was reversed by the intracerebroventricular (ICV) injection of the opiate antagonist naloxone. Similarly, the analgesia produced by a dose of morphine was antagonized by the administration of ACTH or alpha-MSH. The peripheral injection of ACTH or alpha-MSH in normal rats did not increase pain sensitivity. However, ACTH administered ICV increased pain sensivity within 10 min. The results indicate that the pituitary is the source of an endogenous opiate antagonist and hyperalgesic factor and that this factor is ACTH or an ACTH-like peptide. This activity resides in the N-terminal portion of the ACTH molecule since ACTH sub 4-10 is not active in this respect, nor does this activity require a free N-terminal serine since alpha-MSH appears to be almost as potent as the ACTH sub 1-24 peptide. It is concluded that ACTH-like peptides of pituitary origin act as endogenous hyperalgesic and opiate antagonistic factors.
    Keywords: LIFE SCIENCES (GENERAL)
    Type: NASA-TM-81254 , A-8418
    Format: application/pdf
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  • 6
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    Naloxone inhibits and morphine potentiates. The adrenal steroidogenic response to ACTH (1980)
    In:  CASI
    Details
    Publication Date: 2019-06-28
    Description: The adrenal actions were stereospecific since neither the positve stereoisomer of morphine, nor that of naloxone, had any effect on the adrenal response to exogenous adrenocorticotrophic hormone (ACTH). The administration of human beta endorphin to phyophysectomized rats had no effect on the adrenal corticosterone concentration nor did it alter the response of the adrenal gland to ACTH. These results indicate that morphine can potentiate the action of ACTH on the adrenal by a direct, stereospecific, dose dependent mechanism that is prevented by naloxone pretreatment and which may involve competition for ACTH receptors on the corticosterone secreting cells of the adrenal cortex.
    Keywords: LIFE SCIENCES (GENERAL)
    Type: NASA-TM-81253 , A-8416
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  • 7
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    Stress antagonizes morphine-induced analgesia in rats (1981)
    In:  CASI
    Details
    Publication Date: 2019-06-28
    Description: Exposure to restraint stress resulted in antagonism of the analgesic effect of administered morphine in adult male rats. This antagonism of morphine-induced analgesia by restraint stress was not affected by adrenalectomy one day prior to testing, suggesting that stress-induced secretion of corticosteroids is not critical to this antagonism. In addition, parenteral administration of exogenous adrenocorticotropin (ACTH) mimicked the effect of stress in antagonizing morphine's analgesic efficacy. The hypothesis that ACTH is an endogenous opiate antagonist involved in modulating pain sensitivity is supported.
    Keywords: LIFE SCIENCES (GENERAL)
    Type: NASA-TM-81282 , A-8505
    Format: application/pdf
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