The hypophyseal–adrenocortical response to various different stressing procedures in ACTH-treated rats

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Abstract
Twenty-four hours after the last of 14 daily injections of ACTH, the administration of ether, histamine, 1% formalin, or lysine-8-vasopressin produced no rise in the plasma corticosterone level in rats but raised it significantly in saline-treated control animals. As assayed by the plasma corticosterone concentration, ACTH release was found to be inhibited when hypophyseal–adrenocortical responsiveness was not impaired and the peripheral corticosterone level was normal or less than normal. Endotoxin induced nearly the same statistically significant elevation in the ACTH-treated and saline-treated animals. It would appear that it is the high corticosterone level produced by the last ACTH injection that suppresses the corticotrophin-releasing factor (CRF) 24 h later (feedback action) when this level returns to normal or less than normal; and that certain stressors liberate CRF whereas others do not. An explanation for the latter assumption may be found either in the difference in intensity between the stimuli or, more probably, in that the high corticosterone level inhibits the ACTH release mechanism for certain individual stressors, but not for others.