Cortisol receptors

Glucocorticoids. The primary glucocorticoid is cortisol. Receptors for the glucocorticoids are found in all tissues. The overall effects of these hormones include ... 

These effects of CREB and the cortisol-receptor complex are not entirely independent of each other. Each contributes, along with several other transcription factors, to assembling a complex of activator proteins that ultimately determine the level of PEPCK gene expression. 

The hormone cortisol is lip, 17a, 21-trihydroxy-4-pregnene-3,20 dione. It is the major glucocorticoid synthesised and secreted by the human adrenal cortex. Cortisol enters the cell then binds to its receptor. The cortisol-receptor complex enters the nucleus and binds to DNA. 

Effect of glucocorticoid administration on adrenocortical cortisol production (A). Release of cortisol depends on stimulation by hypophyseal ACTH, which in turn is controlled by hypothalamic corticotropin-releasing hormone (CRH). In both the hypophysis and hypothalamus there are cortisol receptors through which cortisol can exert a feedback inhibition of ACTH or CRH release. 

Cortisol/receptor activation causes primary and delayed seomdary responses... 

A potential quality of Trenbolone was its ability to alter cortisol receptors during and after use. The result was cortisol inhibition to some degree on a "semi-permanent" basis and subsequent favorable alteration in the anabolic /catabolic ratio. 

An interesting aspect of all Trenbolone products is their apparent unique ability to permanently shut down existing cortisol receptor-sites. This explains, in part, the exceptional post-cycle lean mass retention realized after protocols utilizing Trenbolones were discontinued. Since Trenbolones are a derivative of Nortestosterone (the active drug in Deca), it should not have been a surprise to realize such exceptional results. 

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.

The glucocorticoid cortisol is secreted from the adrenal cortex as a stress response under the control of adrenocorticotropic hormone (ACTH, corticotropin) produced by the anterior pituitary. Cortisol promotes catabolism by inducing synthesis of specific proteins. Cortisol binds to a cytosolic cortisol receptor which then translocates to the nucleus and switches on the expression of specific genes, notably that for PEP carboxykinase (PEPCK). Cortisol-induced expression of the key gluconeogenesis enzyme PEPCK increases levels of the enzyme and hence increases gluconeogenesis and available blood glucose. The cAMP-and cortisol-mediated pathways for induction of PEPCK expression are further linked by CREB-dependent expression of a coactivator protein PGC-1 that promotes cortisol-dependent expression of PEPCK. 

Receptors — Aldosterone receptor (ALDO-R) Cortisol receptor (CORT-R) ... 

Dang, Z.C., M.H. Berntssen, A.K. Lundebye, G. Flik, S.E. Wendelaar Bonga and R.A. Lock. Metallothionein and cortisol receptor expression in gills of Atlantic salmon, Salmo salar, exposed to dietary cadmium. Aquat. Toxicol. 53 91-101, 2001. 

Pottinger, T. and 1.1. Brierley. A putative cortisol receptor in the rainbow trout erythrocyte stress prevents starvation-induced increases in specific binding of cortisol. J. Exp. Biol. 200 2035 - 2043, 1997. 

Tagawa, M., H. Hagiwara, A. Takemura, S. Hirose and T. Hirano. Partial cloning of the hormone-binding domain of the cortisol receptor in tilapia, Oreochromis mossambicus, and changes in the mRNA level during embryonic development. Gen. Comp. Endocrinol. 108 132-140, 1997. 

Uchida, K., T. Kaneko, M. Tagawa and T. Flirano. Localization of cortisol receptor in branchial chloride cells in chum salmon fry. Gen. Comp. Endocrinol. 109 175-185, 1998. 

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