Adrenocortical cell deletion: The role of ACTH

Adrenocortical cell deletion: The role of ACTH 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 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Pathology Wiley

Adrenocortical cell deletion: The role of ACTH

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Abstract

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

Journal

The Journal of PathologyWiley

Published: Oct 1, 1973

References

  • A suggested explanation for the paradoxically slow growth rate of basal‐cell carcinomas that contain numerous mitotic figures
    Kerr, Kerr; Searle, Searle
  • Autoradiographische Untersuchungen zum Wachstum der Nebennierenrinde der Ratte
    Pappritz, Pappritz; Trieb, Trieb

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