THE ADRENAL GLAND 2/7 



ous or intravenous injection a decrease in adrenal ascorbic acid in nor- 

 mal rats but not in rats 3 days after hypophysectomy. Tlie amounts 

 required are within the physiological range. 



(b) Vogt (11) has also found that epinephrine causes a marked in- 

 crease in the quantity of cortical hormone in the adrenal vein blood of 

 dogs. In chronic experiments, epinephrine produced adrenal hypertrophy 

 only in normal but not in hypophysectomized rats. 



In other words Vogt and ourselves are agreed that epinephrine is a 

 potent stimulus to adrenal cortical secretion, ahhough its exact mechan- 

 ism of action is still unknown. 



It is possible to devise more decisive experiments to settle this point, 

 but whatever may be the answer it is of importance that, either directly 

 or indirectly through the adrenotrophic hormone, the stimulation of the 

 sympathetic nervous system and consequent liberation of epinephrine 

 is capable of increasing cortical hormone output. Such sympathetic ac- 

 tivity is always a component of those varied circumstances that are 

 known to call forth such secretion by the cortex. Heat, cold, hemor- 

 rhage, trauma, burns, toxic agents and painful stimuli of all kinds are 

 always associated with an increased degree of activity of the sympa- 

 thetic nervous system. Consequently it may be assumed that this is at 

 least a very important if not the only means by which an augmented 

 supply of cortical hormone is released to meet these states of emer- 

 gency. 



I am also aware of the implications of the statement that epinephrine 

 can cause stimulation of the adrenotrophic function of the anterior 

 pituitary. For if it is an agent in this regard then it must act either by 

 the stimulation of adrenergic fibers in the anterior lobe, nerve fibers 

 whose existence is equivocal, or directly upon certain sensitive cells in 

 the gland itself, after the manner in which it accelerates glycogenolysis 

 in skeletal muscle. 



(c) A third set of experiments expressing another point of view, or 

 rather another mechanism by which adrenal cortical secretion is regu- 

 lated, has recently been published by Dr. and Mrs. Sayers (12). 



They have found that prior treatment of rats with cortical hormone 

 prevents the usual fall in ascorbic acid when the animals are exposed 

 to cold. We have confirmed this and shown that such treatment also 

 prevents the fall in adrenal ascorbic acid not only after painful stimuli, 

 trauma, etc. but also that produced by epinephrine. I have no doubt that 

 the effect of other types of stress on this component of the adrenal can 

 also be prevented by prior treatment with cortical hormone. Dr. and Mrs. 



