2. Endocrines and Populations 203 



pophysectomy (Farrell ei al., 1955). These results, in addition to those 

 discussed under the relationship between secretory function and zonation 

 of the adrenal cortex, clearly indicate that the secretion of aldosterone is 

 largely independent of adrenocorticotropin and the adenohypophysis and 

 that its responses to ACTH may reflect the increased availability of aldoste- 

 rone precursors from other parts of the cortex. Nevertheless, the secretion 

 of aldosterone in dogs appears to be dependent on an intact pituitary gland 

 (Davis, et al., 1959a). However, as one might expect, a variety of stimuli 

 which produce an increase in the secretion of ACTH may also stimulate 

 an increase in the secretion of aldosterone. Farrell (1958) lists position, 

 surgery, emotional factors, hypertension, insulin shock, and other stimuli 

 among those resulting in an increased secretion of aldosterone, but prob- 

 ably none of these are without an effect on fluid and electrolyte balances 

 which in turn would effect directly the mechanisms regulating the secretion 

 of aldosterone. On the other hand, there is a marked increase in the secre- 

 tion of aldosterone in those diseases which are characterized by striking 

 disturbances in fluid and electrolyte metabolism, such as congestive heart 

 failure, hepatic cirrhosis, and nephrosis (Liddle et al, 1956) . It seems likely 

 that the increase in aldosterone secretion is slight in those circumstances 

 which produce a marked increase in the secretion of ACTH and of the 

 carbohydrate-active corticoids unless there is also involvement of fluid and 

 electrolyte balances. It has been found that only one, the A-1 fraction, of the 

 several distinct fractions of ACTH has an appreciable effect on the secretion 

 of aldosterone, and this fraction is a relatively small proportion of the total 

 amount of ACTH which may be secreted (Farrell et al, 1958; Farrell, 

 1959a) . 



The principal regulation of aldosterone secretion seems to be by a com- 

 bination of neural and neurohumoral factors in response to changes in the 

 volume of extracellular fluid or body potassium. However, there can be 

 little doubt that a hormonal factor is involved in aldosterone secretion, as 

 recently demonstrated with cross-circulation experiments by Yankopoulos 

 et al (1959) . Recent experiments have indicated that the brain may secrete 

 a hormone, glomerulotropin, not as yet isolated and characterized, from the 

 region of the pineal body which stimulates the secretion of aldosterone 

 from the adrenal zona glomerulosa (Farrell, 1959a) . 



Small changes in blood volume can effect striking changes in the rate of 

 secretion of aldosterone (Bartter, 1957) possibly by affecting changes in 

 pulse pressure (Bartter and Gann, 1960). Changes in blood volume elicit 

 maximal reciprocal responses in the secretion of aldosterone and it appears 

 that this system is the most sensitive, as well as the most important, of 

 those involved in the regulation of the secretion of aldosterone (Bartter, 

 1957; Bartter et al, 1959). A rise in blood volume reflexly depresses the 



