Why doesn't hypopituitarism (low ACTH) result in atrophy of Zona Glomerulosa?

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Because ACTH is not necessary for aldosterone synthesis - it directly stimulates cortisol and sex hormone synthesis... so the glomerulosa will keep working and therefore not atrophy.
 
Goljan said it in his audio, but this doesn't make sense to me. What is keeping the ZG from atrophying without ACTH present? (pg 291 of 2011 FA)

The ZG is stimulated by the reinin-angiotensin system as well as ACTH so it would not atrophy. I'm not aware of any hormone other than ACTH that stims the fasiculata and reticularis so they would atrophy.
 
My problem is that I thought Ang II stimulates aldosterone synthase only so that the ZG would atrophy in the absence of ACTH? And I couldn't find anything that said that Ang II is stimulatory on the zona glomerulosa itself...?
 
My problem is that I thought Ang II stimulates aldosterone synthase only so that the ZG would atrophy in the absence of ACTH? And I couldn't find anything that said that Ang II is stimulatory on the zona glomerulosa itself...?
but the zona glomerulosa is where aldo is synthesized...
 
My problem is that I thought Ang II stimulates aldosterone synthase only so that the ZG would atrophy in the absence of ACTH? And I couldn't find anything that said that Ang II is stimulatory on the zona glomerulosa itself...?

Ang II has to logically stimulate the ZG because one of its primary functions aside from vasoconstriction is increasing aldosterone synthesis, which occurs in the zona glomerulosa. ACTH has a much much lower effect on the ZG relative to Ang II so only reticularis and fasiculata would atrophy.
 
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