Adrenergic modulation of adrenocorticotropin responses to insulin-induced hypoglycemia and corticotropin-releasing hormone.

@article{Tomori1989AdrenergicMO,
  title={Adrenergic modulation of adrenocorticotropin responses to insulin-induced hypoglycemia and corticotropin-releasing hormone.},
  author={Naoki Tomori and Toshihiro Suda and Yuriko Nakagami and Fumiko Tozawa and Takashi Sumitomo and Tsuyako Ushiyama and Hiroshi Demura and Kazuo Shizume},
  journal={The Journal of clinical endocrinology and metabolism},
  year={1989},
  volume={68 1},
  pages={
          87-93
        }
}
To study possible adrenergic modulation of pituitary-adrenal responses to insulin-induced hypoglycemia and CRH we examined the effect of nonselective alpha-blockade (phentolamine) and nonselective beta-blockade (propranolol) on plasma ACTH, cortisol, and vasopressin (AVP) responses to hypoglycemia and CRH in five normal men. Infusion of propranolol or phentolamine did not alter basal plasma ACTH or cortisol levels. The propranolol infusion enhanced the stimulatory effect of hypoglycemia on ACTH… 
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References

SHOWING 1-10 OF 29 REFERENCES
Adrenergic control mechanism for ACTH secretion in man.
TLDR
These studies suggest a stimulatory effect of alpha receptors and a possible inhibitory effect of beta receptors on ACTH secretion in man and that either beta adrenergic blockade or alpha stimulation enhances growth hormone secretion, whereas either alpha blockade or beta stimulation sup¬ presses it.
Role of alpha 1- and alpha 2-adrenergic receptors in the growth hormone and prolactin response to insulin-induced hypoglycemia in man.
TLDR
It is concluded that in man alpha-adrenergic stimulation of GH secretion during hypoglycemia is transmitted via alpha 2-receptors, PRL secretion is mediated via alpha 1-receptionors, whereas inhibition of PRL release is mediated through alpha2-reCEPTors.
Hypophysiotropic regulation of adrenocorticotropin secretion in response to insulin-induced hypoglycemia.
TLDR
AVP, not CRF, appears to represent the dynamic mediator of ACTH secretion accompanying insulin-induced hypoglycemia, and this proposal proposes that CRF functions in a permissive role, maintaining a relatively constant portal concentration and thereby allowing expression of the weaker ACTH-releasing activity of AVP and other secretagogues.
Effect of ovine corticotropin-releasing hormone administered during insulin-induced hypoglycemia on plasma adrenocorticotropin and cortisol.
TLDR
Plasma IR-ACTH after insulin alone and insulin plus oCRH rose at the same rate to similar peaks of 258 +/- 14 and 290 +/- 33 pg/mL, respectively, both of which were greater (P less than 0.01) than the peak after o CRH alone and the mean peak plasma IR-cortisol level after insulin plus OCRH (33 +/- 4 micrograms/dL).
THE EFFECT OF PERIPHERAL CATECHOLAMINE CONCENTRATIONS ON THE PITUITARY‐ADRENAL RESPONSE TO CORTICOTROPHIN RELEASING FACTOR IN MAN
TLDR
Results show that modulation of peripheral plasma catecholamine levels within physiological limits does not affect CRF‐stimulated release of ACTH or the adrenal response in normal man.
Evidence for multifactor regulation of the adrenocorticotropin secretory response to hemodynamic stimuli.
TLDR
Observations during atrial pulsation, a stimulus mimicking volume loading and associated with a reduction of systemic ACTH levels, observed a significant decline in portal concentrations of immunoreactive AVP coupled with a nonsignificant trend toward reduced portal Immunoreactive CRF levels, are highly suggestive of multifactor regulatory control of ACTH secretion in response to hemodynamic stimuli.
Effect of adrenaline on basal and ovine corticotrophin-releasing factor-stimulated ACTH secretion in man.
TLDR
It is concluded that circulating adrenaline neither exerts a direct stimulatory effect on pituitary corticotrophs nor enhances the effect of CRF under physiological circumstances.
Pulsatile administration of human corticotropin-releasing hormone in patients with secondary adrenal insufficiency: restoration of the normal cortisol secretory pattern.
TLDR
It is possible that the pulsatile administration of hCRH may prove to be a more physiological technique for restoring adrenal function of patients with corticotroph-sparing secondary adrenal insufficiency and may avoid some of the complications of glucocorticoid administration.
Beta-adrenergic mechanism of insulin-induced adrenocorticotropin release from the anterior pituitary.
TLDR
The results suggest that insulin stimulates ACTH release by a mechanism in which catecholamines of peripheral origin act directly on the anterior pituitary.
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