Effects of Adrenaline on Insulin-Induced Release of Growth Hormone and Cortisol in Man

Müller-Hess, R.; Geser, C. A.; Jéquier, E; Felber, J. P.; A, Vannotti

doi:10.1530/acta.0.0750260

Cited by 9 publications

(5 citation statements)

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“…Muller-Hess, Geser, Jequier et al (1974) and Clutter, Bier, Shah & Cryer (1980) also found that adrenaline infusions did not stimulate cortisol secretion. The finding by Muller-Hess et al (1974) (Sandberg, Nelson, Palmer et al 1953;Ely et al 1954;Hunter et al 1955;Arner, Hedner, Karlefors & Westling, 1963) and various early ACTH bioassays (Vernikos-Danellis & Marks, 1962;Vance & Shioda, 1964) with conflicting results.…”

Section: Discussionmentioning

confidence: 99%

Effect of adrenaline on basal and ovine corticotrophin-releasing factor-stimulated ACTH secretion in man

Al-Damluji¹,

Cunnah²,

Grossman³

et al. 1987

Journal of Endocrinology

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Six normal male subjects were given, in single blind random order on six separate occasions, i.v. bolus doses of synthetic ovine corticotrophin-releasing factor-41 (oCRF-41; 25 and 50 micrograms) with and without adrenaline (3 micrograms/min) i.v. for 150 min, the adrenaline infusions alone and saline placebo. The adrenaline infusions resulted in plasma adrenaline concentrations of 4.33 +/- 0.82 (S.E.M.) nmol/l and were associated with an increase in blood glucose, heart rate and systolic blood pressure and a reduction of diastolic blood pressure. Despite these evident biological effects at several sites, there was no stimulation of plasma ACTH or cortisol by adrenaline in comparison with the effect of saline, and no enhancement of the stimulatory effect of either dose of oCRF-41 on ACTH or cortisol secretion. The ACTH response to 50 micrograms oCRF-41 was greater than that to 25 micrograms, indicating that the 25 micrograms dose of oCRF-41 was submaximal and capable of further enhancement. As the plasma adrenaline concentrations during the adrenaline infusions reached the upper limit of the physiological range of plasma adrenaline in man, yet failed to enhance the ACTH or cortisol responses to a submaximal dose of oCRF-41, we conclude that circulating adrenaline neither exerts a direct stimulatory effect on pituitary corticotrophs nor enhances the effect of CRF under physiological circumstances. The adrenaline infusions attenuated the ACTH and cortisol responses to oCRF-41 and were associated with a transient reduction of basal concentrations of both hormones.

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Section: Discussionmentioning

confidence: 99%

Effect of adrenaline on basal and ovine corticotrophin-releasing factor-stimulated ACTH secretion in man

Al-Damluji¹,

Cunnah²,

Grossman³

et al. 1987

Journal of Endocrinology

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“…However, the transient nature of the adrenal cortical response to persistent hypoglycaemia raises the question as to whether or not activity of the pituitary-adrenal cortical axis is susceptible to some form of adrenergic inhibition. Intravenous infusions of adrenaline in man, in similar amounts to those released endogenously in the calf during severe hypoglycaemia, have been found to suppress the rise in plasma cortisol concentration after insulin (Muller-Hess, Geser, Jequier, Felber & Vannotti, 1974). However, these results could as well be explained by the rise in blood glucose concentration produced by adrenaline under these conditions.…”

Section: -6+0±8mentioning

confidence: 98%

Endocrine responses to insulin hypoglycaemia in the young calf.

Bloom¹,

Edwards²,

Hardy³

et al. 1975

The Journal of Physiology

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SUNMBRY1. Variations in the output of glucocorticoids and catecholamines from the right adrenal gland, in response to insulin hypoglyeaemia, have been investigated in calves 2-5 weeks after birth. These have been correlated with changes in the concentration of glucocorticoids and glucagon in arterial plasma.2. Moderate hypoglycaemia for a limited period (0.1 u. insulin/kg), elicited a prompt increase in steroid output from the adrenal gland followed by a significant rise in plasma glucagon concentration. By comparison, changes in both catecholamine output and peripheral plasma glucocorticoid concentrations were found to be trivial in this group of animals.3. Administration of a larger dose of insulin (0.5 u./kg) produced a more substantial fall in plasma glucose concentration followed by spontaneous recovery within 2-3 hr. This stimulus elicited the release of greater amounts ofboth cortisol and corticosterone, followed by a significant increase both in the output of adrenaline and in plasma glucagon concentration. Increase in steroid output was accompanied byan increase in adrenal blood flow and was associated with elevated concentrations of both steroids in arterial plasma.4. The adrenal cortical response and associated changes in plasma steroid concentration were found to be transient even in response to persistent and intense hypoglycemia (4 u. insulin/kg). The increase in plasma glucagon concentration in this group of animals was not significantly greater than that produced by smaller doses of insulin. However, substantial amounts of adrenaline (78 + 14 ng. kg-1 min-; maximum; n = 9) together with a little noradrenaline (10+3 ng. kg-1 min-'; maximum; n = 9) were released from the right adrenal gland under these conditions. S. R. BLOOM AND OTHERS 5. Changes in adrenal blood flow could be related to adrenal glucocorticoid output in calves given 041 or 0 5 u. insulin/kg. In animals given the largest dose of insulin adrenal blood flow was found to increase coincidentally with rising steroid output but this hyperaemia then persisted after steroid output had subsided to values within the normal range.6. Calves given the largest dose of insulin (4.0 u./kg) invariably collapsed and convulsed after 2-3 hr, but these symptoms could not be related to any particular endocrine response. No clinical signs of hypoglycaemia were observed in the other animals.7. The results are discussed in relation to previous studies of adrenal function in this and other species.

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“…Amphetamines have been shown to stimulate the se cretion of ACTH, cortisol and beta-endorphin (BE) in man by an alpha-adrenergic mechanism [7,14,42] but they have complex pharmacological actions and cause a generalized arousal effect that correlates with the height of the cortisol peak [7,14], so the mechanism by which they stimulate Received: May 22, 1986 Accepted after revision: August 21, 1986 ACTH secretion is uncertain. Studies of directly acting alpha-adrenergic agonists such as epinephrine and norepi nephrine have failed to demonstrate a stimulant effect on ACTH secretion in man [35,49,64]. However, beta-adrener gic agonists have been reported to stimulate the secretion of ACTH and BE in rats in vivo [4,5,30,31,52], while norepi nephrine inhibits corticosteroid secretion in dogs [56].…”

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confidence: 99%

Alpha-Adrenergic Stimulation of Corticotropin Secretion by a Specific Central Mechanism in Man

et al. 1987

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In a double-blind study in normal subjects, methoxamine, a highly selective agonist at alpha-1-adrenoceptors, significantly increased circulating ACTH and cortisol. The stimulant effect of methoxamine on cortisol secretion was dose dependent in the range 3.5–7 µg/kg/min, was abolished by concomitant administration of the strong alpha-1-adrenergic (and weak HI) antagonist thymoxamine but unaffected by the antihistamine, chlorpheniramine. In order to test whether the action of methoxamine on ACTH secretion was exerted centrally or peripherally, the effects of norepinephrine (NE), an alpha-1-agonist that does not cross the blood-brain barrier, were studied. Doses of NE (1–12 µg/min) that increased systolic blood pressure by amounts similar to the changes produced by methoxamine, did not result in any rise in plasma cortisol in normal subjects. The effect of methoxamine, which is more lipid soluble than NE, on plasma ACTH and cortisol, appears to be exerted on the CNS and not at the pituitary or via nonspecific peripheral mechanisms. In addition to its water solubility, NE differs from methoxamine in its beta-1-, beta-2- and alpha-2-agonist actions. However, prenalterol (2 mg) and salbutamol (250 µg), respectively beta-1- and beta-2-adrenergic agonist drugs, had no effect on the secretion of ACTH or cortisol and the alpha-2-antagonist yohimbine in an effective dose did not unmask a stimulant effect of intravenous NE on plasma cortisol. At high infusion rates, NE significantly inhibited cortisol secretion. Stimulation of central alpha-1-adrenergic mechanisms results in secretion of ACTH in man, presumably by increased release of a corticotropin-releasing factor.

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Effects of Adrenaline on Insulin-Induced Release of Growth Hormone and Cortisol in Man

Cited by 9 publications

References 0 publications

Effect of adrenaline on basal and ovine corticotrophin-releasing factor-stimulated ACTH secretion in man

Effect of adrenaline on basal and ovine corticotrophin-releasing factor-stimulated ACTH secretion in man

Endocrine responses to insulin hypoglycaemia in the young calf.

Alpha-Adrenergic Stimulation of Corticotropin Secretion by a Specific Central Mechanism in Man

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