Dutasteride‐mediated morphological changes in the genitourinary tract associated with altered expression patterns of the androgen and estrogen receptors in male rats

So here its showing reduced AR expression.

Dutasteride‐mediated morphological changes in the genitourinary tract associated with altered expression patterns of the androgen and estrogen receptors in male rats

https://onlinelibrary.wiley.com/doi/full/10.1111/andr.12297

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Let me add to this, again here is another case where increased AR expression/overexpression seems like a good thing.
Thoughts?

Key targets of hormonal treatment of prostate cancer. Part 1: the androgen receptor and steroidogenic pathways

1.use intracellular androgens more efficiently (AR amplification, AR protein overexpression, AR hypersensitivity)
2.mechanisms that utilize steroids from the circulation more efficiently through altered gene expression

Just so im clear on the wordage,
“The biological activity of androgens is thought to occur predominantly through binding to intracellular androgen-receptors”

What about this?

Key targets of hormonal treatment of Post Finasteride Syndrome. Part 1: the androgen receptor and steroidogenic pathways

1.Use intracellular androgens more efficiently (AR amplification, AR protein overexpression, AR hypersensitivity)
2.Gain mechanisms that utilize steroids from the circulation more efficiently through altered gene expression

Going back to the first post, heres a thought right here.

Another important point of this study is that we identified that dutasteride caused the expression changes of AR and ER in penile tissue as well as prostatic tissue. Similar to AR, ERs are known to express in male organs especially in reproductive tract (Zhou et al ., 2002). ERs have two subtypes, alpha and beta, and both subtypes of ERs are known to have important role in male reproductive tract biology (Nie et al ., 2002). In this study, we revealed that dutasteride caused the decreased AR expression and increased ER beta expression in rat penis. We considered that the changes in AR and ER beta expression are mainly because of changes in tissue DHT levels, because there were no changes in AR and ER beta expression only in bladder where no tissue DHT concentration changes were observed. These expression changes in hormonal receptors have been reported in cases after castration. Niu et al ., (2003) reported that the expression of AR in the prostate increased rapidly after castration and then dropped to a lower level than that of pre‐castration.

That second part, even some early anti-androgens were also partial AR agonists.
Here might be the crash or false sense of improvement when its really not.
Even when some recommend going back on Fin, you could get a short term boost in AR activity.
Its a type of resistance.