214 /. /. Christian 



intimate association with nerve fibers of the supraopticohypophyseal tract. 

 These vessels drain into the adenohypophysis, where they break up to 

 form a series of sinusoids. Here they are joined by capillaries from the 

 systemic arterial supply. The direction of the flow is from the median 

 eminence to the adenohypophysis. Neural fiber tracts from hypothalamic 

 nuclei descend through the median eminence and give off branches which 

 terminate in intimate association with the arterial portal plexus in the 

 median eminence (Scharrer and Scharrer, 1954). The remaining fibers 

 continue on their way, to terminate in close approximation to capillaries 

 in the neurohypophysis. Neurosecretory material is believed to traverse 

 the sheaths of these nerves from hypothalamic secretory nuclei (Scharrer 

 and Scharrer, 1954; Rennels and Drager, 1955). There is evidence that a 

 fraction of this neurosecretory material is responsible for stimulating the 

 release of ACTH from the anterior pituitary (Drager, 1955; Rothballer, 

 1953; Saffran et al., 1955). Evidently the material is released by the appro- 

 priate stimulus from the terminations of the neurosecretory fibers into the 

 pituitary portal vessels and is then borne, via the portal system, to the 

 cells of the adenohypophysis proper (Scharrer and Scharrer, 1954; Rennels 

 and Drager, 1955). It is generally accepted that no nerve fibers terminate 

 in the adenohypophysis and that there are no direct neural, only vascular, 

 connections between the adenohypophysis and neurohypophysis (Green, 

 1951). The identity of the hypothalamic corticotropin-releasing factor 

 (CRF) has not been determined, although it appears to be a small protein 

 often associated with Pitressin (Saffran et al., 1955; Porter and Rumsfeld. 

 1956). One group of investigators believes that the ACTH-releasing ac- 

 tivity is associated with Pitressin, in particular with its pressor activity 

 (ADH, vasopressin) (McCann, 1957; jMcCann and Fruit, 1957). ADH 

 exerts a powerful antidiuretic action on the kidney at many times the 

 dilution that is necessary for it to exert a pressor effect or to stimulate the 

 release of the ACTH (McCann and Fruit, 1957) . It has been suggested for 

 this reason that the concentration of ADH, when it is released from the 

 posterior pituitary into the systemic circulation, is sufficient to effect anti- 

 diuresis, but insufficient to stimulate the release of ACTH, but that when 

 it is released directly into the pituitary portal circulation, it reaches the 

 adenohypophysis in a sufficient concentration to effect the release of ACTH 

 (McCann and Fruit, 1957). It should be noted that ADH evidently is 

 released simultaneously into the pituitary portal system from the hypothal- 

 amus and from the neurohypophysis into the systemic circulation in re- 

 sponse to stimulation. 



Nevertheless, as attractive as this theory may seem, good evidence is 

 accumulating from a number of sources which indicate's that the corti- 

 cothopin-releasing factor is an entity separate from vasopressin, although 



