Resistance to Epinephrine Stress in the Dog.

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Abstract
Current concepts of the physiologic activation of the pituitary-adrenal mechanism suggest that epinephrine is the humoral agent responsible for the release of ACTH from the anterior pituitary. It is not known whether epinephrine acts directly on the anterior pituitary or by stimulating the hypothalamus. Other evidence suggests that epinephrine released as a result of sympathico-adrenal discharge may act peripherally to increase the tissue utilization of 11-oxysteroids, leading to lowered plasma levels and activation of the anterior pituitary to release ACTH. It has been demonstrated that repeated exposure to a single stress results in the development of a stage of resistance to that stress. In view of the importance of epinephrine as a possible physiologic activator of the pituitary-adrenal mechanism, it was of interest to determine whether a "resistance" could be experimentally produced to epinephrine in the dog. The eosinophil response was used as a criterion of adrenal cortical discharge. Epinephrine was admd. daily in doses of 5-10 [mu]g./kg./min. intraven. for 60 min. to unanesthetized, trained dogs, in an attempt to produce a state of resistance. Animals that developed a resistance to epinephrine were exposed to ACTH and other stresses (e.g., glucose, histamine, cold, starvation) in an attempt to elucidate the mechanism of epinephrine refractoriness. The repetitive daily admn. of epinephrine in the dog resulted in a progressively diminished eosinopenic response. During the state of epinephrine resistance, there was neither a depletion of endogenous ACTH nor an exhaustion of the adrenal cortex. Adaptation of the organism to epinephrine stress with decreased tissue utilization of corticoids seemed to most satisfactorily explain the phenomenon of epinephrine resistance. Demonstration of resistance to epinephrine speaks against epinephrine as the only physiologic stimulus for the continuous secretion of ACTH.
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