Naloxone inhibits and morphine potentiates the adrenal steroidogenic response to ACTH

Heybach, John P.; Vernikos, Joan

doi:10.1016/0014-2999(81)90337-x

Cited by 23 publications

(7 citation statements)

References 19 publications

(14 reference statements)

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“…In rat adrenal cell culture experiments, administration of opioid peptides resulted in corticosterone production, which was diminished by naloxone . In vivo , morphine potentiated and naloxone inhibited corticosterone production in hypophysectomized rats . If similar mechanisms exist in humans, a pattern of low morning cortisol, blunted ACTH‐stimulated cortisol and loss of diurnal rhythm could occur during chronic opioid exposure.…”

Section: Discussionmentioning

confidence: 93%

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Adrenal insufficiency in patients on long‐term opioid analgesia

Gibb

Stewart

Walker

et al. 2016

Clinical Endocrinology

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Section: Discussionmentioning

confidence: 93%

“…16 In vivo, morphine potentiated and naloxone inhibited corticosterone production in hypophysectomized rats. 17 If similar mechanisms exist in humans, a pattern of low morning cortisol, blunted ACTH-stimulated cortisol and loss of diurnal rhythm could occur during chronic opioid exposure.…”

Section: Discussionmentioning

confidence: 99%

Adrenal insufficiency in patients on long‐term opioid analgesia

Gibb

Stewart

Walker

et al. 2016

Clinical Endocrinology

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“…In another study, intravenous injection of 3END or intraperitoneal injection of either morphine or naloxone in hypophysectomized rats had no effect on corticosterone content of the adrenal gland (33). However, morphine potentiated and naloxone inhibited the response of corticosterone to ACTH (33). Aldosterone was not measured in these experiments.…”

Section: Resultsmentioning

confidence: 84%

“…Although Met-enkephalin did not have an effect in this system, administration of ACTH 2 h after Met-enkephalin caused a 34% greater increase in corticosterone release than the same dose of ACTH added before Met-enkephalin. In another study, intravenous injection of 3END or intraperitoneal injection of either morphine or naloxone in hypophysectomized rats had no effect on corticosterone content of the adrenal gland (33). However, morphine potentiated and naloxone inhibited the response of corticosterone to ACTH (33).…”

Section: Resultsmentioning

confidence: 93%

Beta endorphin selectively stimulates aldosterone secretion in hypophysectomized, nephrectomized dogs.

Güllner¹,

Gill²

1983

J. Clin. Invest.

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A B S T R A C T We examined the effects of synthetic human /-endorphin (BEND) and a stable methionine (Met)-enkephalin analogue on aldosterone and cortisol secretion rates in anesthetized, hypophysectomized, and nephrectomized dogs and compared them to those of (1-39) ACTH. The circulation of the adrenal glands was completely isolated on the arterial and venous sides (Hilton Pouch). The peptides were infused to deliver 3 pmol/min into the aortic "pouch." Blood was collected from the vena caval pouch, which received blood only from the adrenal gland. Secretion rates of aldosterone and cortisol were calculated as the product of adrenal blood flow and venous steroid concentration. Duplicate steroid measurements were obtained during a control period, at 10, 30, and 50 min of peptide infusion and during a postcontrol period. BEND increased aldosterone secretion rate from 2.4±0.5 ng/ min (mean±SEM) to 3.2±0.9 ng/min at 10 min (N.S.), 8.2±2.5 ng/min (P < 0.05) at 30 min and 11.0±3.7 ng/ min (P < 0.05) at 50 min of infusion. Cortisol secretion rate was not affected by infusion of SEND. Infusion of the stable Met-enkephalin analogue D-alanine2; Metphenylalanine4, Met(O)-enkephalin-ol or saline alone had no effect on aldosterone or cortisol secretion rates. ACTH infusion increased mean aldosterone secretion rate by -215% and significantly stimulated cortisol secretion rate. These results indicate that BEND selectively stimulates aldosterone secretion with a potency similar to that of an equimolar dose of ACTH. INTRODUCTION There is considerable indirect evidence suggesting that an unidentified pituitary factor other than ACTH

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“…The corticotropin releasing action of morphine is mainly mediated via the hypothalamus; lesions of the median eminence blocks the adrenal cortical response to morphine (George and Way, 1959;Kokka and George, 1974). Recently morphine has been demonstrated to potentiate the adrenal steroidogenic response to corticotropin (Heybach and Vernikos, 1981). However, the release by morphine opiates of vasopressin may also play an important role in the secretion of corticotropin (DeBodo, 1944;George and Way, 1959;Inturrisi and Fujimoto, 1968;Meites et al, 1979;Koyuncuo~lu et al, 1984 b).…”

Section: Commentsmentioning

confidence: 99%