ACTH endocrine system

Endocrine system Morphine and other opioid analgesics stimulate the release of vasopressin and prolactin and inhibit the release of luteinizing hormone, ACTH and follicle stimulating hormone. 

ENDOCRINE SYSTEM A number of endocrine tissues respond to PGs. In a number of species, the systemic administration of PGE increases circulating concentrations of adrenocorticotropic hormone (ACTH), growth hormone, prolactin, and gonadotropins. Other effects include stimulation of steroid production by the adrenals, stimulation of insulin release, and thyrotropinlike effects on the thyroid. The critical role of PGF in parturition relies on its ability to induce an oxytocin-dependent decline in progesterone levels. PGE works as part of a positive-feedback loop to induce oocyte maturation required for fertihzation during and after ovulation. 

In the 1950s, Guillemin and Rosenberg, and Saf an and Schally discovered that hypothalamic extracts that could stimulate the release of ACTH from anterior pituitary cells. This represented another connection between the brain and the endocrine system. CRF is the major regulator of the baseline and stress-induced release of ACTH, P-endorphin, and other proopiomelanocortin-derived peptides from the anterior pituitary. 

Such events show how the immune, endocrine and central nervous systems are integrated in their responses to any form of stress. It is well established that physical or psychosocial stress causes increased secretions of prolactin, growth hormones, thyroid, and gonadal hormones, in addition to ACTH. Endogenous opioids are secreted under such conditions and function as immunomodulators, while also elevating the pain threshold. Receptors for such hormones exist on immunocompetent cells, along with receptors for catecholamines, serotonin and acetylcholine. 

Figure 18.2. Endocrine-immune inter-relationship in normal subject. The hypothalamic-pituitary-adrenal (HPA) axis is a feedback loop that includes the hypothalamus, the pituitary and the adrenal glands. The main hormones that activate the HPA axis are corticotrophin releasing factor (CRF), arginine vasopressin (AVP) and adrenocorticotrophic hormone (ACTH). The loop is completed by the negative feedback of cortisol on the hypothalamus and pituitary. The simultaneous release of cortisol into the circulation has a number of effects, including elevation of blood glucose for increased metabolic demand. Cortisol also negatively affects the immune system and prevents the release of immunotransmitters. Interference from other brain regions (e.g. hippocampus and amygdala) can also modify the HPA axis, as can neuropeptides and neurotransmitters.

The effect of stress on the endocrine and immune systems depends upon its duration and severity. Following acute stress, the rise in ACTH in response to the release of corticotrophin releasing factor (CRF) from the hypothalamus results in a rise in the synthesis and release of cortisol from the adrenals. The increase in the plasma cortisol concentration results in a temporary suppression of many aspects of cellular immunity. Due to the operation of an inhibitory feedback mechanism, stimulation of the central glucocorticoid receptors in the hypothalamus and pituitary causes a decrease in the further release of CRF, thereby decreasing the further... 

Figure 18.3. Endocrine-immune inter-relationship in depression. In depression, the hypothalamic-pituitary-adrenal (HPA) axis is up-regulated with a down-regulation of its negative feedback controls. Corticotrophin releasing factor (CRF) is hypersecreted from the hypothalamus and induces the release of adrenocortico-trophic hormone (ACTH) from the pituitary. ACTH interacts with receptors on adrenocortical cells and cortisol is released from the adrenal glands adrenal hypertrophy can also occur. Release of cortisol into the circulation has a number of effects, including elevation of blood glucose. The negative feedback of cortisol to the hypothalamus, pituitary and immune system is impaired. This leads to continual activation of the HPA axis and excess cortisol release. Cortisol receptors become desensitized leading to increased activity of the pro-inflammatory immune mediators and disturbances in neurotransmitter transmission.

In fact, ACTH secretion is regulated by a neuro-hormonal mechanism and a humoral feedback mechanism. The neurohormonal control of ACTH secretion involves what has been referred to as a third-order neuroendocrine mechanism. Three steps are involved in this control. A stimulus (stress, for example) brings the central nervous system to secrete a hormone (CRF), which acts on another endocrine structure in the anterior lobe of the hypophysis where it induces the secretion of second hormone (ACTH), which ultimately acts on the target endocrine gland—the adrenal cortex [40, 56-60]. 

---