Effect of Exogenous Arginine Vasopressin on Adrenocorticotropin and Cortisol Release in Myotonie Dystrophy Patients: Delayed Responses of Normal Magnitude

Grice, Jeffrey E.; Jackson, J A; Hewett, M. J.; Penfold, Paula J.; Jackson, Richard V.

doi:10.1111/j.1365-2826.1991.tb00240.x

Cited by 7 publications

(2 citation statements)

References 22 publications

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“…The results of these studies are therefore consistent with a CRHmediated mechanism of action of naloxone in humans. This conclusion is also supported by other in vivo studies on patients with myotonic dystrophy, who show an in creased ACTH response to oCRH [48], a delayed ACTH response of normal magnitude to exogenous AVP [49], and an increased, non-delayed (and therefore CRH-like) ACTH response to naloxone [50].…”

Section: Discussionsupporting

confidence: 76%

A Synergistic Adrenocorticotropin Response to Naloxone and Vasopressin in Normal Humans: Evidence That Naloxone Stimulates Endogenous Corticotropin-Releasing Hormone

et al. 1995

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Naloxone stimulates pituitary-adrenal function by blocking an endogenous inhibitory opioidergic tone which modulates pituitary adrenocorticotropin (ACTH) release. In animals, this action of naloxone is mediated by increased corticotropin-releasing hormone (CRH) secretion, but such a mechanism is disputed in humans. CRH and arginine vasopressin (AVP) are known to have a synergistic effect on ACTH secretion in both humans and animals. In vitro, this synergism is independent of L-type voltage-dependent Ca²⁺ channel function. The aims of this study were therefore: (i) to determine if the combined administration of naloxone and AVP is synergistic regarding ACTH release; (ii) to assess the effect of nifedipine, which blocks L-type Ca²⁺ channels, on the ACTH response to combined naloxone/AVP stimulation. Seven healthy volunteers were studied using a placebo-controlled, single-blind protocol. Naloxone (125 µg/kg) and/or AVP (10 units) were given in all four possible combinations, and oral nifedipine (20 mg) was also given with naloxone and AVP as an additional test. The mean AUC and the mean peak change in ACTH levels following combined naloxone/AVP administration were both significantly greater than the arithmetic sum of the ACTH responses to naloxone and AVP given on separate occasions (AUC: 1,576.4 ± 417.9 vs. 567.1 ± 106.1 pmol·min·Hp < 0.002; peak change: 37.9 ± 14.0 vs. 11.8 ± 2.0ρmol/l, p < 0.007). Nifedipine reduced the ACTH response to combined naloxone/AVP stimulation by 43% (AUC: 1,576.4 ± 417.9 vs. 897.0 ± 186.2; p < 0.05), but it remained greater than the sum of the individual responses (897.0 ± 186.2 vs. 567.1 ± 106.1, p < 0.05). These results indicate that naloxone and AVP cause a synergistic ACTH response, and that this synergy is not abolished by nifedipine. They also provide evidence that naloxone stimulates the human hypothalamic-pituitary-adrenal axis predominantly or exclusively via increased release of endogenous CRH.

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Section: Discussionsupporting

confidence: 76%

A Synergistic Adrenocorticotropin Response to Naloxone and Vasopressin in Normal Humans: Evidence That Naloxone Stimulates Endogenous Corticotropin-Releasing Hormone

et al. 1995

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“…Dystrophia myotonica (DM) patients demonstrate an exaggerated ACTH response to ovine CRH (Jackson et al, 1988), but an ACTH response of normal magnitude to AVP (Grice et a[., 1991). These patients have an exaggerated ACTH response to naloxone .…”

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confidence: 99%

Naloxone‐induced ACTH release: mechanism of action in humans

Jackson

Grice

Hockings

et al. 1995

Clinical Endocrinology

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Hyperkalaemia and selective hypoaldosteronism in myotonic dystrophy*

Misra

DeSilva

Fellerman

et al. 2002

Clinical Endocrinology

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Myotonic dystrophy (MyD) is a common genetic neuromuscular disorder in which chromosome 19 gives rise to an abnormal expansion of CTG-trinucleotide repeats. MyD is a highly variable multisystem disorder with muscular and nonmuscular abnormalities. Increasingly, endocrine abnormalities, such as gonadal, pancreatic, and adrenal dysfunction are being uncovered. Herein we present three unrelated cases with MyD with abnormally elevated serum potassium; 2 of the 3 cases presented clinically with cardiac dysrhythmias. Hyperkalaemic conditions such as renal failure, cortisol deficiency, pseudohyperkalaemia, and hyperkalaemic periodic paralysis were excluded. Further endocrine evaluation revealed baseline hypoaldosteronism associated with elevated renin activity. Perturbation of the renin-angiotensin-aldosterone system resulted in appropriately enhanced renin activity but with a subnormal aldosterone response, which appeared to be due to adrenal hyporesponsiveness. The treatment of all cases with fludrocortisone was without effect. Whether the apparent mineralocorticoid abnormality in MyD is due to associated hormonal perturbations (i.e. excessive ACTH responsiveness. elevated cytokines, elevated atrial natriuretic hormone, etc.), adrenal atrophy, and/or a manifestation of the underlying kinase dysfunction is uncertain, but merits further evaluation in view of the clinical consequence of hyperkalaemia.

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Effect of Exogenous Arginine Vasopressin on Adrenocorticotropin and Cortisol Release in Myotonie Dystrophy Patients: Delayed Responses of Normal Magnitude

Cited by 7 publications

References 22 publications

A Synergistic Adrenocorticotropin Response to Naloxone and Vasopressin in Normal Humans: Evidence That Naloxone Stimulates Endogenous Corticotropin-Releasing Hormone

A Synergistic Adrenocorticotropin Response to Naloxone and Vasopressin in Normal Humans: Evidence That Naloxone Stimulates Endogenous Corticotropin-Releasing Hormone

Naloxone‐induced ACTH release: mechanism of action in humans

Hyperkalaemia and selective hypoaldosteronism in myotonic dystrophy*

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