Cortisol vasopressin, effect

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.

Figure 18.5. Endocrine-immune relationship following chronic stress. In chronic stress, the hypothalamic-pituitary-adrenal (HPA) axis is up-regulated with a down-regulation of its negative feedback control. Arginine vasopressin (AVP) is secreted from the hypothalamus and induces the release of adrenocorticotrophic 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. Unlike in acute stress, the negative feedback of cortisol to the hypothalamus and pituitary 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.

It has been suggested that the postpituitary hormones may play an important role in antipituitary stimulation. Low doses of vasopressin had no effect on the adrenal venous concentration of cortisol when injected into the internal carotid artery but had an effect when placed in the adrenal artery (E3). 

Nicotine binds selectively to the nicotinic receptors that are present in the adrenal medulla, brain, autonomic ganglia, and neuromuscular junctions. It causes the release of several neurotransmitters and hormones such as acetylcholine, norepinephrine, dopamine, serotonin, arginine vasopressin, j3-endorphin, adrenocorticotropic hormone, and cortisol (187). This neuro-regulatory effect of nicotine is dose-dependent and occurs as plasma nicotine level rises when tobacco is smoked. The neurotransmitters released in the brain medi-... 

Cortisol secretion by isolated adrenal pouches in hypoxed dogs was stimulated by cyclic AMP, vasopressin and ACTH O. However, epinephrine and norepinephrine, which stimulate formation of cyclic AMP in fat pads, dichloroisoproterenol, which inhibits adenyl cyclase, or dihydroergota-mine, an inhibitor of action of cyclic AMP in the liver, failed to have any effect. 

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