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PubMed1992

Structure and dynamics of adrenal mitochondria following stimulation with corticotropin releasing hormone.

The mitochondria of rat adrenals were investigated qualitatively and quantitatively in different functional states of the adrenal cortex. Following stimulation of the animals with corticotropin releasing hormone (CRH), the corticosterone serum levels reached a maximum 1 hour after stimulation with CRH. The amount of inner mitochondrial membrane within the zona fasciculata increased showing a biphasic time course, with a first maximum 2 hours and a second maximum 8 hours after stimulation. In contrast, a significant rise of mitochondrial volume occurred only 24 hours after CRH stimulation. Therefore, the dense vesicularization of mitochondrial cristae may constitute an early process to enhance the steroidogenic capacity of these cells. Within cells of the transition zone between zona glomerulosa and zona fasciculata, we could depict a special type of mitochondria with characteristic crescent-like cristae only seen after stimulation with CRH. This type of mitochondria may represent an intermediate form between mitochondria of zona glomerulosa and zona fasciculata underlining the impressive transformational capacity of adrenocortical mitochondria. After hypophysectomy, zona fasciculata cells contained mitochondria with tubular inner membranes, representing a hypofunctional state. In contrast, the hypofunctional state after hypophysectomy and the hyperfunctional state after stimulation of the adrenal cortex via CRH injection did not appear to correlate with the morphology of mitochondria from the zona reticularis and adrenal medulla.

Adrenal Cortex↗
PubMed1974

Glucocorticoid induced stress susceptibility in swine: adrenocortical pathology.

The studies reported here were undertaken to better characterize the role of the adrenal cortex in the increased susceptibility to stress observed in porcine stress syndrome. Since adrenal hypofunction was suggested during early studies as a factor in events leading to porcine stress syndrome it was decided to produce such a state by the exogenous administration of the glucocorticoids prednisolone and fluoroprednisolone.A total of 34 pigs (weighing 90 to 100 kg) received a series of graded doses (given intramuscularly) of one or the other of the foregoing compounds and were necropsied 48, 72, and 120 hours after the last treatment. The major adrenocortical changes produced by these treatments were atrophy, an accentuation of degenerative changes which could be observed in milder form in many of the 30 control pigs examined, a marked increase in stainable lipid 120 hours after the last fluoroprednisolone treatment and, ultrastructurally, an increase in lysosome-like bodies and cellular debris ("myelin bodies").Adrenocortical atrophy is not a feature of porcine stress syndrome nor were the localized depositions of stainable lipid within the zona reticularis, described in porcine stress syndrome, found in the glucocorticoid treated pigs. Consequently, the findings reported here bear a somewhat limited resemblance to those observed in pigs affected by porcine stress syndrome and cast some doubt on whether adrenal hypofunction plays a role in the pathogenesis of the latter condition.

Adrenal Glands↗