I found this and thought it was interesting. Not sure if this has been posted.
HPA dysfunction in the form of hypoactive HPA axis or hypocortisolism -
Two similar studies by M. Kabbaj et al showed that chronic treatment with alpha 1 antagonist prazosin reduced hippocampal corticosteroid receptors and increased cort. response to stress. In particular, high responder rats did were not affected, but low responder rats, which had increased brain MR/GR and more efficient negative feedback, were affected (decreased cort. receptors and increased cort. response). In the other study, rats adrenalectomized and sub. with cort. who were treated with praz. chronically, showed a reduction in hippocampal MR levels, while adrenal-intact rats showed a reduction in hippocampal GR, and enhanced cort. responses following stress.
Another study was done where chronic treatment with prazosin to early abstinent alcoholics for 5 weeks seemed to reverse the blunted HPA response to stressors.
After 5 weeks with the alpha 1 antagonist, the praz. group was tested with stressors and showed a robust cort. response, in comparison to the placebo group which showed blunted response. It is said that HPA dysfunction in early abstience is marked by blunted HPA responses to stress and this increases relapse risk. The author of the study attributed the cort. response to higher NA levels as a response to blockade, but did not consider the possibility that maybe praz. was somehow affecting CRh or hippocampal corticosteroid receptors involved in the feedback system. The two groups showed identical cort levels prior to stress test, and only the praz. group produced healthy cort responses to the stressors.
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Many veterans with PTSD use this drug and find it to be helpful for aspects of their condition, mainly helping to sleep and have less nightmares.
What does chronic blockade of alpha-1 adrenergic receptors do to the HPA axis? Could it be helpful in the hypoactive HPA observed in many cases, such as CFS, PTSD where enhanced negative feedback is one of the key features.
I spoke with one of the researchers of the two studies done on the rats, and they said that this drug does show promise in HPA dysfunction, but there is no money for more studies, or studies on humans. this is an old drug, and its already being used in PTSD simply because NA drive is observed to be hyperactive in PTSD.
[DLMURL]http://pubget.com/paper/17552999/Individual_differences_in_the_effects_of_chronic_prazosin_hydrochloride_treatment_on_hippocampal_mineralocorticoid_and_glucocorticoid_receptors[/DLMURL]