Posted by sregan on October 5, 2006, at 20:28:57
In reply to Re: **CORTISOL**, posted by SLS on October 5, 2006, at 18:21:34
>A glucocorticoid receptor antagonist should INCREASE circulating glucorticoids because if the receptors are blocked then the monitoring mechanism thinks they are LOW and need to be increased? So it actually increases CRH->cortisol?
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> Exactly. I would expect adrenal exhaustion as a possibility if treatment were continued for too long. I'm not sure, though.
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> - ScottI just read that the GC is an inhibitory receptor and in animal studies of chronic stress GCs become stimulatory rather than inhibitory on HPA axis.
In the normal model GC/MR stimilation from plasma glucortocoids causes an inhibitory effect on CRH. For HPA dysfunction in the chronic stress model antagonising the GC receptor makes sense as glucortocoids are causing a stimulatory effect perpetuating the cycle.
poster:sregan
thread:558802
URL: http://www.dr-bob.org/babble/20061003/msgs/692211.html