STUDIES ON THE MECHANISM OF STIMULATION OF ACTH SECRETION WITH THE AID OF MORPHINE AS A BLOCKING AGENT<sup>1</sup>

Briggs, F. Norman; Munson, Paul L.

doi:10.1210/endo-57-2-205

Cited by 136 publications

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“…This result was in marked contrast to those obtained by Briggs and Munson (1955). These different results are probably due to the measurements used as indicators of ACTH release or due to the different sex of the experimental animals.…”

Section: Discussioncontrasting

confidence: 89%

“…In the rats pretreatment with morphine was shown by Briggs and Munson (1955) to prevent the fall in adrenal ascorbic acid elicited by surgical stress such as dissection of the bile duct. The operation, which took 2 min to perform, caused maximal loss of adrenal ascorbic acid in rats deeply anesthetized with pentobarbital, but morphine (2 mg./100g.…”

Section: Discussionmentioning

confidence: 99%

“…Previously, Briggs and Munson (1955) found pentobarbital-morphine treatment in rats to be effective against such non-specific stresses as surgical operation, histamine and vasopressin which are associated with ACTH release as evidenced by adrenal ascorbic acid depletion. Furthermore, these investigators have reported that morphine alone, four daily injections without pentobarbital, was capable of inhibiting the response of the anterior pituitary to histamine stress.…”

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confidence: 99%

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Acute Effect of Morphine Administration on Secretion of Adrenal Corticosterone in Rats

1970

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SynopsisThe purpose of this study is to determine the acute effect of morphine on ACTH secretion and to determine whether morphine has a direct action on the adrenal cortex by the adult female Wistar rat. ACTH was measured by the determination of corticosterone levels in adrenal glands, adrenal venous blood and circulatory blood. It should be emphasized that in this paper, mechanism of secretion of adrenal corticosterone by the acute effect (the early stage action) following morphine administration was described. Even in morphinization with five daily morphine (2mg/100g, B. W., i. p.) injections, the account of acute effect was determined immediately after the final injection of morphine administration. Morphine alone can not act as an inhibitor of ACTH release nor as an inhibitor of ACTH release due to histamine stress, and morphinization can not act to inhibit ACTH release or to block the effect of a histamine stress on the secretion of ACTH in the early stage action of the final morphine administration, as evidenced by corticosterone levels both in adrenal glands and in circulating blood of the intact rats. Morphine (2mg/100g,B. W., i. p.) alone caused stimulation of ACTH release as well as the final morphine injection of morphinization, and pretreatment of the rats with morphine(2mg/100g, B. W., i. p.) could not act to block the effect of a histamine (0.5 mg/ 100g, B. W., i. p.) stress on the release of ACTH in the early stage action of morphine administration. A detailed account of the effect of morphine or morphinization with four daily morphine injections on corticosterone levels both in adrenal and in adrenal venous blood of the hypophysectomized-ACTH-treated rat has been reported. Morphine (2mg/100g, B. W., i. p.) alone or with pretreatment of pentobarbital (1mg/100g, B. W., i.p.) does not directly interfere with the response of the adrenal cortex to exogenous ACTH in the early stage action of morphine administration. Morphinization with four daily morphine (2mg/100g, B. W., i. p.) injections in the early stage action following the directly act on adrenal corticoidogenesis in vivo. These results suggest in the early stage action of morphine administration that morphine acts to stimulate ACTH release at a higher level than the anterior pituitary and does not directly act on adrenal cortex, and that the acute effect of strong stimuli on the rate of ACTH release is not mediated by a decrease in the concentration of circulating adrenal corticosteroids.

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Section: Discussioncontrasting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

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Acute Effect of Morphine Administration on Secretion of Adrenal Corticosterone in Rats

1970

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“…This result obtained by systemic administration may not negate the direct effect of morphine on the adrenal cortex, as Lymangrover et al (1981) and Meites (1984) have reported that opioids, as well as naloxone, may act directly on the adrenal cortex as well as on the hypothalamus. Briggs and Munson (1955) and Gibson et al, (1979) reported that morphine inhibited the stress-induced ACTH secretion. On the other hand, Buckingham and Cooper (1984) have reported that morphine exaggerated the stress-induced CRF secretion in the hypothalamus and the ACTH secretion from the anterior pituitary in their bioassay system.…”

Section: Resultsmentioning

confidence: 99%

Effect of morphine on hypothalamic corticotropin-releasing factor(CRF) and pituitary-adrenocortical activity.

1986

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The effects of intraperitoneal and intra-third ventricular administration of morphine on the hypothalamic corticotropin-releasing factor (CRF) and the pituitary-adrenocortical activity were examined in unanesthetized, freely moving rats.Hypothalamic CRF was measured by rat CRF radioimmunoassay. Intraperitoneal or intra-third ventricular administration of morphine increased blood concentrations of ACTH and corticosterone while intraperitoneal administration tended to increase CRF concentration in the whole hypothalamus including the median eminence and intra-third ventricular administration increased CRF concentration in the hypothalamus excluding the median eminence.However, morphine seemed to inhibit the increase in CRF concentration in the hypothalamus induced by the ether-laparotomy stress. The main site of morphine action on the hypothalamo-pituitary-adrenocortical system seemed to be in the hypothalamic area.

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“…Morphine administration has been shown to stimulate corticosterone secretion and adrenal gland function (Briggs and Munson, 1955). This response has been presumed to be mediated solely by the hypothalamic-pituitary axis or by a direct action at the pituitary (Kokka and George, 1974;Lotti et al, 1969;Zimmerman and Critchlow, 1973).…”

Section: Discussionmentioning

confidence: 99%

Naloxone inhibits and morphine potentiates the adrenal steroidogenic response to ACTH

Heybach

Vernikos

1981

European Journal of Pharmacology

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STUDIES ON THE MECHANISM OF STIMULATION OF ACTH SECRETION WITH THE AID OF MORPHINE AS A BLOCKING AGENT¹

Cited by 136 publications

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Acute Effect of Morphine Administration on Secretion of Adrenal Corticosterone in Rats

Acute Effect of Morphine Administration on Secretion of Adrenal Corticosterone in Rats

Effect of morphine on hypothalamic corticotropin-releasing factor(CRF) and pituitary-adrenocortical activity.

Naloxone inhibits and morphine potentiates the adrenal steroidogenic response to ACTH

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STUDIES ON THE MECHANISM OF STIMULATION OF ACTH SECRETION WITH THE AID OF MORPHINE AS A BLOCKING AGENT1

Cited by 136 publications

References 0 publications

Acute Effect of Morphine Administration on Secretion of Adrenal Corticosterone in Rats

Acute Effect of Morphine Administration on Secretion of Adrenal Corticosterone in Rats

Effect of morphine on hypothalamic corticotropin-releasing factor(CRF) and pituitary-adrenocortical activity.

Naloxone inhibits and morphine potentiates the adrenal steroidogenic response to ACTH

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STUDIES ON THE MECHANISM OF STIMULATION OF ACTH SECRETION WITH THE AID OF MORPHINE AS A BLOCKING AGENT¹