Glucocorticoids rapidly inhibit oxytocin-stimulated adrenocorticotropin release from rat anterior pituitary cells, without modifying intracellular calcium transients.

Abstract

Glucocorticoid hormones suppress the secretion of ACTH evoked by secretagogues such as CRF and arginine vasopressin. In this study, we investigated the effects of glucocorticoids on ACTH release induced by oxytocin (OT) and on intracellular free calcium ion levels in corticotropes prepared from the adenohypophyses of female Wistar rats.Pulsatile additions of physiological concentration of OT (10 nM) to superfused anterior pituitary cells caused pulsatile ACTH release about 4-fold above basal secretion with similar peak amounts of ACTH du ring subsequent OT pulses. Exposure of the cells to corticosterone (100 nM) or to a selective glucocorticoid receptor agonist RU 28362 (100 nM) for 30 min suppressed OT-stimulated but not basal ACTH release by approximately 60%. Inhibition gradually disappeared during subsequent pulses of OT in the absence of corticosterone. Pretreatment with I

Administering an Appeasing Substance to Improve Performance, Neuroendocrine Stress Response, and Health of Ruminants

“…Stress may also be defined from a physiological standpoint as an immediate activation of the hypothalamic–pituitary–adrenal (HPA) axis following the perception of a stressor [ 4 ], characterized by the synthesis and release of corticotropin-releasing hormone (CRH) and vasopressin (VP) by the hypothalamus [ 2 ]. In cattle, CRH is more potent than VP, ultimately leading to the activation of the pituitary gland-mediated release of adrenocorticotropic hormone (ACTH) [ 5 ]. Corticotrophs located in the anterior pituitary gland are responsible for the production of ACTH, which, in turn, stimulates the synthesis and release of steroids by the adrenal gland, and promotes cholesterol uptake [ 2 ].…”

REVIEW: Oxytocin: Crossing the Bridge between Basic Science and Pharmacotherapy

“…The ACTH response due to oxytocin can be variable, that is, oxytocin exerts a synergistic or additive effect on ACTH secretion when applied with CRH or vasopressin, respectively [54]. Oxytocin-dependent stimulation of ACTH release is mediated by an increase in [Ca 2+ ] i , which occurs in the absence of external Ca 2+ [54,56] by mobilizing Ca 2+ from InsP 3 -sensitive intracellular Ca 2+ stores [57]. Furthermore, this ACTH release induced by oxytocin is blocked by glucocorticoids (corticosterone or RU 28362, a selective glucocorticoid receptor agonist) without interfering with [Ca 2+ ] i transients [57].…”

“…Oxytocin-dependent stimulation of ACTH release is mediated by an increase in [Ca 2+ ] i , which occurs in the absence of external Ca 2+ [54,56] by mobilizing Ca 2+ from InsP 3 -sensitive intracellular Ca 2+ stores [57]. Furthermore, this ACTH release induced by oxytocin is blocked by glucocorticoids (corticosterone or RU 28362, a selective glucocorticoid receptor agonist) without interfering with [Ca 2+ ] i transients [57]. Subsequently in the literature, no further emphasis was placed on better understanding the effect of oxytocin on ACTH secretion.…”

Patterns of ACTH Secretagog Secretion in Response to Psychological Stimuli

“…An interesting implication for any physiological role for OT is evidence that release may be resistant to glucocorticoid feedback inhibition (28,29,173,186,187). Other studies, however, indicate that corticosterone may, in fact, inhibit OT's ability to induce ACTH secretion (188). The cross-species relevance of a secretagog function for OT is unclear since OT is generally thought to have an inhibitory role in primates instead of a facilitory role in rodents (52,(155)(156)(157).…”