Oxytocin: Major Corticotropin-Releasing Factor Secreted from Diabetes insipidus Rat Posterior Pituitary <i>in vitro</i>

Abstract

In diabetes insipidus (DI) rats, electrical stimulation of the posterior pituitary lobes in vitro promotes the release of corticotropin-releasing factor (CRF). The CRF activity is abolished by preincubation of the posterior lobe media with thioglycolate. Oxytocin, which is released concomitantly into the medium (3.2 mIU/lobe/20 min), accounts for the complete CRF effect. Neural lobe extracts from DI and normal rats contain 40–70% more CRF activity than can be explained by their content in vasopressin and/or oxytocin. The discrepancy between released and extracted CRFs suggests that hypothetical CRFs or potentiating factors are not released from nerve endings or have to be present in high concentrations to manifest their effect.

Oxytocin at physiological concentrations evokes adrenocorticotropin (ACTH) release from corticotrophs by increasing intracellular free calcium mobilized mainly from intracellular stores. Oxytocin displays synergistic or additive effects on ACTH-releasing factor or arginine vasopressin-induced ACTH secretion, respectively.

“…Available evidence suggests that OT serves as an ACTH-releasing factor in the AVP-deficient Brattleboro rat (45). Moreover, previously reported data also reveal that OT in certain kinds of stress is involved in the regulation of ACTH secretion, supporting the con- (11,15), the release of ACTH was not saturated but increased in a dose-dependent manner up to 10 .uM, the highest concentration tested.…”

Oxytocin at physiological concentrations evokes adrenocorticotropin (ACTH) release from corticotrophs by increasing intracellular free calcium mobilized mainly from intracellular stores. Oxytocin displays synergistic or additive effects on ACTH-releasing factor or arginine vasopressin-induced ACTH secretion, respectively

“…9, 43, 44) into hypophyseal portal blood in the regulation of ACTH secretion is intriguing. Available evidence suggests that OT serves as an ACTH-releasing factor in the AVP-deficient Brattleboro rat (45). Moreover, previously reported data also reveal that OT in certain kinds of stress is involved in the regulation of ACTH secret.ion, supporting the con- cept of a multifactorial modulation by the hypothalamus (21,42).…”

Pituitary Portal Plasma Levels of Oxytocin during the Estrous Cycle, Lactation, and Hyperprolactinemia

“…Recently, new OT-containing fiber systems have been identified in the median eminence [1][2][3][4] and have been implicated in the control of prolactin (PRL) and adrenocorticotropin (ACTH) secretion from the anterior lobe of the pituitary gland. [5][6][7][8][9][10][11][12] This paper summarizes experimental findings that evaluate the hypophysiotropic function of median eminence OT by characterizing neuropeptide secretion into the blood of pituitary portal vessels under physiological conditions when the secretion of PRL is known to be altered.…”