202 J. J. Christian 



accompanying adrenalectomy. However, adrenalectomized wild Norway 

 rats (Rattus norvegicus) cannot be maintained in this fashion, even with 

 the NaCl content of the drinking water as high as 4 %(Richter et al., 1950) . 

 These facts emphasize the wide divergence between laboratory and wild 

 strains of the same species. Evidently the requirements for adrenocortical 

 hormones are much greater in mammals under feral conditions than for 

 those raised or maintained in the laboratory or zoo. There is a marked 

 disparity in the adrenal weights of mammals raised in the laboratory and 

 in the same species under natural conditions, the differences due largely to 

 differences in the amount of cortical tissue (Rogers and Richter, 1948; 

 Nichols, 1950; Christian and Ratcliffe, 1952; Christian, 1955a) ; some of this 

 difference, however, may be associated with the unconscious selection in 

 breeding colonies for docility and good breeding performance. 



(2) Regulation of aldosterone secretion} Since aldosterone acts pri- 

 marily to maintain fluid and electrolyte homeostasis, it is not surprising 

 that the secretion of this hormone is regulated largely by these factors. 

 Changes in the volume of extracellular fluid (probably mainly the intra- 

 vascular volume) , and the level of body potassium affect the rate of aldo- 

 sterone secretion (Liddle et al., 1956; Bartter, 1957; Bartter et at., 1959), 

 but to some extent the secretion of aldosterone in vivo can be stimulated 

 by adrenocorticotropin (Farrell et al., 1955; 1958; Liddle et al., 1956), but 

 apparently not in vitro (Stachenko and Giroud, 19596). This discrepancy 

 may be explained by the increased production of the precursors of aldoste- 

 rone by the f asciculata which then become accessible to the zona glomerulosa 

 in the intact adrenal. Even though the secretion of aldosterone is mode- 

 rately stimulated by ACTH, the stimulation is not maintained in spite of 

 continued treatment with ACTH (Liddle et al., 1956), and the response is 

 considerably less than that seen following changes in the volume of extra- 

 cellular fluid or in body potassium (Bartter et al., 1959). The glomerulosa 

 will respond to increased ACTH with increased secretion of aldosterone for 

 only about 3 or 4 days, and then the rate of secretion declines in spite of 

 continued ACTH and reaches base levels or even lower levels of secretion 

 in about a week (Liddle et al., 1956). After this period, continued ACTH 

 will not increase the secretion of aldosterone (Bartter et al., 1959). Finally, 

 the secretion of aldosterone is only slightly depressed by suppressing ACTH 

 secretion (Farrell et al., 1955; Liddle et al., 1956; Bartter, 1957) or by hy- 



' Since completion of this chapter, there has been marked progresses in understanding 

 the regulation of aldosterone secretion in response to hemodynamic changes. It is fairly 

 certain that in response to decreased arterial pressure there is increased relea.se of renin 

 from the kidney. The end product of this release is angiotensin II which, in the presence 

 of basal levels of ACTH, stimulates aldosterone secretion. [For a review see J. (). Davis 

 (1963).] 



