154 



PHYSIOLOGICAL TRIGGERS 



cellular uterine water may have been preceded by an acute redistribution of its 

 electrolyte pattern (41). 



In view of the implication of secretions of the adrenal cortex in the regulation 

 of osmotic phenomena, it seemed advisable to determine whether these early 

 indices of estrogen activity might be subject to modification by the activity of 

 the pituitary-adrenal system. It was found (35) that the increase in uterine 

 weight produced 4 hours after the intravenous administration of estradiol could 



10 20 30 40 50 

 HOURS ARER ESTROGEN 



10 20 30 

 HOURS AFTER 



Fig. I. Influence of lime after estrogen administration on weight and water content of the 

 uterus of the castrated rat. Tolal lieiglU of bars represents the average uterine wet weight; 

 cross-hatched portion, uterine dry weight; crosses, % uterine water. Each point represents the 

 mean =h the standard error of values obtained from at least 7 animals, except at 96 hours where 

 only 4 determinations were made of uterine water content. In the case of the bars, only the 

 positive segment of the standard error is shown. All animals except the untreated control 

 group at o hours, were injected intravenously with 0.5 /xg estradiol- 17 /? per 100 gm body 

 weight. Estrogens were administered as sodium salts in saline, prepared as previously de- 

 scribed (23). Autopsy was performed at the times indicated. (Reprinted from ref. 36 by per- 

 mission of the editor and publishers.) 



Fig. 2. Influence of time after estrogen injection on oxygen consumption in vitro and water 

 content of the uterus of the castrated rat. Each point represents the mean =fc the standard 

 error of values obtained in 6-66 experiments. Open circles, first hour oxygen consumption in 

 medium without added glucose; solid circles, oxygen consumption in medium with added 

 glucose; crosses, % uterine water. Dosage of estradiol, 0.5 ixg/ioo gm body weight, injected 

 intravenously. (Reprinted from ref. 25 by permission of the editors.) 



be completely prevented by the concurrent injection of ACTH (adrenocortico- 

 trophic hormone). The adrenocortical steroids found (32) to be the most active 

 in reproducing the ACTH effect were Cortisol and cortisone (Kendall's Com- 

 pounds F and E, respectively). Cortisol appeared to be the most effective 

 steroid in this regard, and in other respects as well, and was chosen for most of 

 the subsequent studies (cf. 36). Thus, the 17-hydroxy and ii-oxy functions 

 appeared to be necessary for the highest activity. As will be discussed below, the 



