2. Endocrines and Populations 225 



tivity, achieving the latter by diminishing the sensitivity of the arterial 

 musculature to epinephrine and norepinephrine by maintaining a constant 

 low level of pressor amines in the arterial wall (Burn and Rand, 1958a, b). 

 The source of the norepinephrine in the arterial walls is apparently the 

 chromaffin tissue including the adrenal medulla, or sympathetic neural 

 terminations which appear to release a low level of these cathechols amines 

 constantly into the circulation (Bell et al., 1950; Gaddum and Holzbauer, 

 1957). Experiments with reserpine (Burn and Rand, 1958a, b; Eranko 

 and Hopsu, 1958) , which depletes the epinephrine and norepinephrine from 

 the adrenal medulla and sympathetic chromaffin tissue, depletes the con- 

 tent of catechol pressor amines from the arterial walls and thereby makes 

 them excessively sensitive to circulating epinephrine and norepinephrine. 

 However, the arteries are unresponsive to other noncatechol pressor amines 

 which apparently exert their usual effects by releasing the norepinephrine in 

 the arterial walls (Burn and Rand, 1958a, b). There is also evidence that 

 the adrenal carbohydrate-active corticoids have a part m the maintenance 

 of arterial tonus and reactivity by increasing the sensitivity of the vascula- 

 ture to the action of epinephruie and norepinephrine (Ramey and Gold- 

 stein, 1957) . 



Reserpine is a pharmacologic agent which causes the disappearance of 

 the catechol pressor amines from the chromaffin tissue and subsequently 

 from the arteries (Burn and Rand, 1957, 1958b), but stimulation of the 

 sympathetic nervous system also can exhaust the pressor amines from the 

 sympathetic ganglia and adrenal medulla, although the stimulus must 

 persist for 30 minutes or longer to achieve exhaustion of the adrenal medul- 

 las of dogs (Gaddum and Holzbauer, 1957). Therefore, it is conceivable 

 that prolonged and intense emotional stimuli, such as one might expect as 

 a result of social interactions between animals in populations of excessive 

 density, might exhaust the stores of pressor amines, especially in the sub- 

 ordinate animals. If such an event occurs, one might anticipate that there 

 would be a subsequent depletion of the arterial norepinephrine and loss of 

 arterial tonus which might account for the occasional deaths due to the 

 shock seen in mice shortly after they are first placed together (Christian, 

 1955b) or following more protracted periods of social strife (Frank, 1953). 

 A loss of vascular tonus with a subsequent hypotension, and eventually 

 shock with circulatory collapse, could explain the symptoms observed by 

 Frank (1953) in dense populations of Microtus in the wild or in captivity 

 or might be a part of the picture of "shock disease" (Green and Larson, 

 1938; Green et al, 1939; Christian and Ratcliffe, 1952). There is also the 

 possibility of a simultaneous exhaustion of readily available glucose re- 

 serves by the action of epinephrine, especially in animals with a high 

 metabolic rate, or, perhaps more likely, a loss of the ability to mobilize 



