Neuroendocrine and cardiovascular parameters during simulation of stress-induced rise in circulating oxytocin in the rat

Abstract

Physiological functions of oxytocin released during stress are not well understood. We have (1) investigated the release of oxytocin during chronic stress using two long-term stress models and (2) simulated stress-induced oxytocin secretion by chronic treatment with oxytocin via osmotic minipumps. Plasma oxytocin levels were significantly elevated in rats subjected to acute immobilization stress for 120 min, to repeated immobilization for 7 days and to combined chronic cold stress exposure for 28 days with 7 days immobilization. To simulate elevation of oxytocin during chronic stress, rats were implanted with osmotic minipumps subcutaneously and treated with oxytocin (3.6 microg/100 g body weight/day) or vehicle for 2 weeks. Chronic subcutaneous oxytocin infusion led to an increase in plasma oxytocin, adrenocorticotropic hormone, corticosterone, adrenal weights and heart/body weight ratio. Oxytocin treatment had no effect on the incorporation of 5-bromo-2-deoxyuridine into DNA in the heart ventricle. Mean arterial pressure response to intravenous phenylephrine was reduced in oxytocin-treated animals. Decrease in adrenal tyrosin hydroxylase mRNA following oxytocin treatment was not statistically significant. Oxytocin treatment failed to modify food intake and slightly increased water consumption. These data provide evidence on increased concentrations of oxytocin during chronic stress. It is possible that the role of oxytocin released during stress is in modulating hypothalamic-pituitary-adrenocortical axis and selected sympathetic functions.

Oxytocin Affects Nitric Oxide and Cytokine Production by Sepsis-Sensitized Macrophages

“…The anti-inflammatory effect of OXT may also be related to its participation in the regulation of the hypothalamic pituitary-adrenal axis. OXT potentiates the release of ACTH and the increase in corticosterone/cortisol levels [19,29,30]. In addition, OXT secretion is considered to promote insulin and glucagon secretion, and thus to regulate the peripheral metabolism during infection [27].…”

Behavioral and neuroendocrine consequences of juvenile stress combined with adult immobilization in male rats

“…Animals The immobilization (IMO) stress was conducted by gently restraining the animal in a prone position and taping its four limbs to metal mounts attached to a wooden board. This procedure was originally described by Kvetnansky and Mikulaj (1970), and it has been used in several labs (Nostramo et al, 2012;Nostramo et al, 2013;Ondrejcakova et al, 2010;Tillinger et al, 2013). In our group, the procedure has been adapted to minimize the movement of the animal and therefore the probability to induce inflammation in the paws.…”

Prolonged oxytocin treatment in rats affects intracellular signaling and induces myocardial protection against infarction

“…Thus, increased activation of both p38-MAPK and Hsp27 protein observed in the present study may indicate involvement of these proteins in cardioprotective potential of oxytocin. Moreover, increased activation of p38-MAPK pathway may be, at least partially, responsible for oxytocin-induced increase in the heart weight without apparent enhancement of cell proliferation observed in our previous study (Ondrejcakova et al 2010). Kobayashi et al (2009) demonstrated an increase in phosphorylated ERK in the hearts of rabbits injected with oxytocin postinfarction.…”

“…Oxytocin may be considered a typical stress hormone responding to several acute and chronic stress stimuli and has a great array of physiological activities in the periphery (Jezova et al 1995;Ondrejcakova et al 2010). Cardiovascular system belongs to important targets of oxytocin action that is supported by the presence of oxytocin receptors in the heart (Gutkowska et al 1997) and vascular endothelial cells (Thibonnier et al 1999;Jankowski et al 2000).…”