PLATES LV-LVII WITH the exception of the zona glomerulosa, the adrenal cortex responds to adrenocorticotrophin (ACTH) by both hypertrophy (Moon, 1936-37) and hyperplasia (Farese, 1968). Conversely, withdrawal of ACTH causes a diminution of the size of the adrenal cortex (IngIe, Higgins and Kendall, 1938; Miller, 1950; LaMont, 1964, cited by Symington, 1969) which has long been considered to be due to atrophy of some cells and deletion of others (Deane and Greep, 1946; Bransome and Reddy, 1963). The intracellular events determining atrophy are not known precisely, but there is morphological evidence that this process involves reversal of the changes induced by ACTH. Thus, cytoplasmic volume decreases (Deane and Greep; Chester Jones, 1950); profiles of smooth endoplasmic reticulum become less numerous (Borowicz, 1965) and mitochondrial numbers and surface area diminish (Nishikawa, Murone and Sato, 1963; Canick and Purvis, 1972). By contrast, practically nothing is known of the mechanism and morphological manifestations of cell deletion after ACTH withdrawal; indeed, the existence of such a process has been denied (Smith, 1930; Messier and Leblond, 1960). The evidence for it to date is rather inconclusive, deriving from observations of degenerative intracellular changes which are of doubtful specificity and occur late after hypophysectomy
The Journal of Pathology – Wiley
Published: Oct 1, 1973
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