The Effect of Oxytocin Infusion on Adenohypophyseal Function in Man

Abstract

The responses of the adenohypophyseal hormones adrenocorticotrophin (ACTH), growth hormone (GH), thyroid stimulating hormone (TSH), prolactin, luteinizing hormone (LH) and follicle stimulating hormone (FSH) to sub-maximal doses of hypothalamic releasing factors were studied in six lean male volunteers (age 23-35 years) with and without infusions of oxytocin (OXT). OXT infusion (mean plasma concentration 133.6 +/- 2.6 pmol/l) completely inhibited the plasma ACTH responses to corticotrophin releasing hormone (CRH) (saline, peak increment ACTH 1.61 +/- 0.75 pmol/l; OXT, peak increment ACTH - 0.04 +/- 0.28 pmol/l; P less than 0.05). OXT infusion had no significant effect on the GH response to growth hormone releasing hormone (GHRH), the TSH and prolactin responses to thyrotrophin releasing hormone (thyroliberin, TRH) or the LH and FSH responses to gonadotrophin releasing hormone (luteoliberin, GnRH). The data support a role for OXT in the modulation of ACTH secretion in man.

Review: Central non-glucocorticoid inhibitors of the hypothalamo-pituitary-adrenal axis

“…When last reviewed by , the literature suggested stimulatory effects of OT on ACTH release in rodents and inhibitory effects in humans. Support for the latter has been reinforced by a report that CRH-induced ACTH release was completely inhibited by an OT infusion in normal human subjects (Page et al 1990), which suggests a direct effect on the pituitary since OT probably does not cross the blood-brain barrier in significant amounts. An inhibitory effect of OT in rats has also been reported in a model permitting rapid automated blood sampling in which the corticosterone response to a noise stress was attenuated by central infusion of OT, but not AVP (Windle et al 1997).…”

Signals for nausea and emesis: Implications for models of upper gastrointestinal diseases

“…Studies in rat show elevated plasma cortisol levels with the production of CFA (Smotherman, 1985). Additionally (as mentioned above), there are many potential candidate hormones that might contribute to nausea, including vasopressin, oxytocin, adrenaline, growth hormone, prolactin, adrenocorticotrophic hormone, and pancreatic polypeptide (Eversmann et al, 1978;Feldman et al, 1988;Nussey et al, 1988;Page et al, 1990;Xu et al, 1993). However, the challenge with all the systemic signals for nausea is to understand where and how they gain access to the central nervous system (e.g.…”

“…Despite a focus on vasopressin secretion as a correlate of nausea (and oxytocin as a correlate of malaise in the rat) other hormones are increased in subjects with nausea induced by apomorphine, ipecac, and motion, including adrenaline, cortisol, growth hormone, prolactin, adrenocorticotrophic hormone, and pancreatic polypeptide (Eversmann et al, 1978;Feldman et al, 1988;Nussey et al, 1988;Page et al, 1990;Xu et al, 1993). It remains to be determined whether any of these hormones are related to the genesis for the sensation of nausea in contrast to being indicators of the generally "stressful" nature of malaise.…”

Oxytocin in the human--regulation of derivations and destinations

“…Stimulated responses have also been suppressed. Oxytocin reduced ACTH which was stimulated by insulin-induced hypoglycaemia, by vasopressin (96) or by CRH (97). Investigations in which ACTH rises were not sensitive to oxytocin have also been reported (98,99).…”

“…In the human female oxytocin increased thyrotrophin-releasing hormone-induced prolactin release, but seems not to have a similar effect in the male (97).…”