Feedback Mechanisms Regulating Pituitary ACTH Secretion in Rats Bearing Transplantable Pituitary Tumors1

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Abstract
The corticoid feedback mechanism was studied in rats bearing an ACTH-producing tumor (MtT-F4). At various times after tumor implantation, there was a direct relationship between increase in adrenal weight and blood corticosterone levels, and between the decrease in anterior pituitary weight and ACTH content. Plasma ACTH remained near normal until about 6 weeks after implantation. In spite of very high blood corticosterone levels and an 83% reduction in pituitary ACTH content at this time, stress caused a doubling in the circulating ACTH level which was completely abolished by hypo-physectomy. Tumor implantation 1 day prior to adrenalectomy prevented the increase in the resting level of ACTH in the blood and the rise in pituitary ACTH content that occurs 3 weeks after adrenalectomy. It is concluded that inhibition of ACTH secretion by maximal endogenous levels of blood corticoids is slow to develop. Under conditions when such high levels of blood corticoids persist for a considerable length of time, the response to stress is not completely prevented. Furthermore, in the absence of corticoids, an extrapituitary source of ACTH may inhibit adenohypophysial ACTH synthesis and secretion.