2. Endocrines and Populations 237 



investigators (Gerwing, 1958; Gerwing et al., 1958) conclude that the 

 hypothesis of a reciprocal relationship between the secretion of TSH and 

 ACTH by the anterior pituitary is compatible with the evidence for rats, 

 mice, and rabbits, but not for guinea pigs and monkeys. They suggest that 

 in the latter two the inhibitory effect of increased corticosteroids does not 

 occur. However, we have seen that the corticosteroids probably have no 

 effect in the inhibition of TSH release and thyroid function in rats and 

 rabbits in response to alarming stimuli; so that some other explanation 

 must be sought. Man is probably similar to guinea pigs and rhesus monkeys 

 in the above responses of the thyroid (Gerwing et al., 1958) . These studies 

 emphasize the importance of careful comparative work as well as the im- 

 portance of dose-time relationships in physiologic functions in different 

 species of mammal. 



Starvation causes a profound depression of thyroid activity, probably 

 by suppressing the secretion of TSH, as it has been shown that acute starva- 

 tion markedly depresses the blood level of TSH in mice and rats (Monej'-, 

 1955). However, if starved animals are subjected to cold, the degree of 

 thyroid depression is inversely related to the degree of the reduction in 

 environmental temperature (Reichlin, 1957a). The thyroidal iodine release 

 rates at the lower temperatures, even though reduced, are appreciably 

 higher than they are in starved animals at higher temperatures. The mainte- 

 nance of body temperature appears to take precedence over the conserva- 

 tion of nutritive reserves and tissues in the regulation of thyroid activity 

 activity (Reichlin, 1957a). 



In contrast to some of the above relationships, increased thyroidal ac- 

 tivity increases adrenocortical activity in white rats (Wallach and Reineke, 

 1949). Administration of thyroxine decreases adrenal ascorbic acid to 

 minimal levels after 2-4 days and is followed, upon continued treatment 

 with adequate doses of thyroxine, by a progressive increase in adrenal size 

 and ascorbic acid content which reaches maximum in 4 weeks. The in- 

 crease in adrenal weight in these circumstances is roughly proportional to 

 the dose of administered thyroxine. There is a narrow dose range of thyrox- 

 ine in which there is no effect on the adrenals. Perhaps this dose range repre- 

 sents the normal physiologic daily secretion rate. It may be that 'the 

 adrenal hypertrophy observed in rats exposed to cold is in part a result of 

 the increased thyroid activity. On the other hand, adrenocortical function 

 does not seem to depend on the presence of a normally functional thyroid, 

 as thyroidectomy does not cause adrenal atrophy in rats although the zona 

 fasciculata is reduced in width (Hess, 1953), nor does thyroidectomy de- 

 crease the ability of the adrenals to respond to stress (Hess and Finerty, 

 1952) . The adrenals of rats treated with antithyroidal compounds (thioura- 

 cil) also (were) responsive to injected adrenocorticotropin (Freedman and 



