BIOLOGICAL TRANSPORT 



growth. A number of ordinary amino acids have their concentra- 

 tions in the uterus approximately doubled in 24 hours but apparently 

 not in 4 hours after estradiol is given, according to Kalman and Lom- 

 brozo (1961). Transports are often modified together by the same 

 agency; in this case an acceleration of urea entry into the uterus has 

 also been recorded recently (Kalman et al., 1961). Other uterine 

 transport changes will probably also be found to be produced by 

 estrogens. 



The inhibition of hexose passage across the human red blood 

 cell membrane by stilbestrol has already been discussed. The same 

 agent, together with estradiol, estradiol disulfate, and stilbestrol 

 disulfate, also inhibits phosphate entry into red cells (Christensen 

 and Jones, 1961). Under special conditions, estradiol disulfate stimu- 

 lates the mediated uptake of uric acid by these cells. The disulfates 

 of estradiol and stilbestrol at 1-m/W levels stimulate amino acid ac- 

 cumulation by the Ehrlich cell (Christensen, 1960b). Other steroids 

 are less active on the red blood cell membrane; e.g., rather high levels 

 of corticosterone are required to inhibit fructose uptake (Pletscher 

 et al., 1955). Estradiol also increases, and testosterone decreases, the 

 renal excretion rate of the rat for the model amino acids, a-amino- 

 isobutyric and 1-aminocyclopentanecarboxylic acids (Riggs and 

 Walker, 1962). These actions taken together imply widespread 

 sensitivity of transports to steroids. 



Physiologically significant hormone actions may perhaps occur 

 only when the membrane has binding sites with sufficient affinity to 

 fix a steroid present at the relatively low physiological levels; per- 

 haps this site must also be appropriately close to the solute-trans- 

 porting site. 



Glucocorticoids on hepatic amino acid uptake 



Trauma or fever are known to lower the plasma amino acids. 

 Laparotomy in rats was shown to produce this action, and at the 

 same time to increase the hepatic concentrations of amino acids 

 (Christensen et al., 1948). The injection of hydrocortisone (or, less 

 effectively, of cortisone) quickly produces the same effect. For this 

 purpose the model amino acid, a-aminoisobutyric acid, was used 

 to restrict other possible sources of the change in distribution (Noall 

 et al, 1957; Christensen, 1960a; Kaplan and Nagareda, 1961). The 

 suggestion has been made that (a) the catabolic effect of the gluco- 

 corticoids, (b) their gluconeogenic effect, and (c) their stimulation 



96 



