Nervous System Mechanism for Epinephrine Secretion

Abstract

Summary

These experiments indicate the existence of an inhibitory central mechanism, located in the region of the brain bounded by the superior colliculi and the optic chiasm, which influences epinephrine secretion from the adrenal glands. The existence of a central mechanism in the spinal cord, which exercises an opposite influence to that of this cerebral centre, was established earlier.² Removal of the influence of the brain centre, results in epinephrine output from the adrenals at the maximum rate of spontaneous liberation which can be sustained through the physiological activity of the spinal cord centre. This rate corresponds with the upper limit of the range of normal epinephrine secretion.¹

Despite the fact that epinephrine was the first hormone to be isolated from its source, and to be synthesized, the functional significance of epinephrine secretion is still obscure. Physiological interpretations from pharmacological observations often have been misleading. Only quantitative experiments, yielding results within the limits of the physiological rate of liberation, can be expected to yield unequivocal information on the function of epinephrine secretion.

In the light of the experiments reported herewith, it can be seen why reflex augmentation of the rate of epinephrine secretion has not been demonstrated successfully in animals under the influence of asphyxia⁸ or stimulation of sensory nerve trunks.⁹ For, even if these stimuli might affect appropriate receptors, which could alter the rate of epinephrine secretion, there is no reason to assume that they might not equally influence the cerebral and the cord centres, thus defeating the possibility of eliciting reflexly either augmentation or diminution in the rate of epinephrine secretion from the adrenal glands. In preliminary tests, it was not found possible to elicit augmentation of the epinephrine output by stimulation of sensory nerves, following mechanical destruction or compression of the brain.^9a