Because of the complex physiologic interactions of hypothalamus, pituitary, thyroid, and gonads with the adrenal gland, other exogenous toxicants and experimental manipulations that directly damage these tissues or modulate their secretory functions can result in secondary effects in the adrenal cortex, including atrophy. Cortical atrophy can also be a direct effect of exogenous toxicants that interfere with normal adrenocortical steroidogenesis and/or the physiologic effects of the renin-angiotensin system on the adrenal. Atrophy can also result from more direct ACTH deficiency, such as may occur with abnormal pituitary function. The glandular capsule may be thickened due to fibrosis (Ĭauses of adrenal cortical atrophy in rats and mice include any factor that increases levels of glucocorticoids, such as exogenous administration or endogenous hypersecretion by a functional adrenocortical neoplasm in the same or contralateral gland, which secondarily results in decreased adrenocorticotropic hormone (ACTH) levels. There is variably decreased overall size of the gland, often with distortion of the gland outline. The zonae fasciculata and reticularis are more often affected than the zona glomerulosa. ), the atrophic cortex is characterized by reduced thickness of the one or more of the cortical layers due to a decrease in cell size or a loss of cells. Compared with the normal adrenal cortex (
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