204 /. /. Christian 



secretion of aldosterone via stretch receptors in the region of the right 

 striiim or adjacent vena cava (Davis ct al., 1956, 1957, 1958; Liddle ct al., 

 1956; Bartter et al, 1958, 1959; Farrell, 1959a; Anderson et al, 1959), the 

 vagus nerve (Mills et al, 1958), and central pathways possibly to depress 

 the secretion of glomerulotropin from the pineal region of the brain al- 

 through Davis et al (1959b) indicated that the vagus is not involved in the 

 afferent pathways of this control. Conversely, a decrease in blood volume 

 stimulates the secretion of aldosterone (Bartter et al, 1959), although the 

 exact pathways and mechanism by which this is achieved is unknown. 

 Bartter and Gann (1960) have suggested that pulse pressure is a factor in 

 changes in blood volume which affects aldosterone secretion. A drop in 

 pulse pressure stimulates the release of aldosterone and a rise inhibits its 

 release. These changes apparently come about through changes in the rate 

 of tonic impulses over receptor nerves in the region of the thyrocarotid 

 artery. 



Another system that regulates the secretion of aldosterone involves the 

 levels of potassium in the body. A deficiency of potassium, therefore a 

 lowered concentration of body potassium, results in a lower rate of secretion 

 of aldosterone if it was originally elevated, whereas an increase in body 

 potassium results in an increase in the secretion of aldosterone (Bartter, 

 1956; Bartter et al, 1959). A rise in serum potassium, either absolute or 

 relative to the concentration of sodium, is associated with an increase in the 

 secretion of aldosterone, but it is not known whether a fall m potassium 

 actively inhibits its secretion or permits it to return to base levels passively 

 (Farrell, 1958) . It has been shown that these changes in the rate of secre- 

 tion of aldosterone in response to changes in body potassium are inde- 

 pendent of sodium concentration in the serum or the total amount of so- 

 dium in the body and are also independent of the sodium: potassium ratio 

 in the serum (Bartter, 1956; 1957; Bartter et al, 1959). Similarly, there is 

 no evidence to suggest that altered renal hemodynamics are responsible for 

 the altered secretory rates of aldosterone (Bartter et al, 1956; Cole, 1957). 

 It is not known yet whether the regulation of the secretion of aldosterone by 

 the body potassium is directly on the cells of the adrenal zona glomerulosa 

 or is mediated through central channels (Bartter, 1956; Bartter ct al, 1959) . 

 It cannot be said whether serum potassium, intracellular potassium, or a 

 combination of both effects the control of the secretion of aldosterone, but 

 there is evidence that the adrenal cortical cells themselves may respond 

 directly to this type of stimulus (Bartter, 1956) . On the other hand, Farrell 

 (1958) suggests that the effect is through central channels. However, 

 changes in potassium are not as important in the regulation of the secretion 

 of aldosterone as changes in the volume of the extracellular fluid (Bartter, 

 1957; Bartter efaL, 1959). 



