Abstract

Abstract Extracellular sodium ion was found to be needed for the maximum uptakes of α-aminoisobutyric acid, l-alanine, l-proline, and 1-aminocyclopentanecarboxylic acid by the immature rat uterus in vitro. The stimulation of uptakes of these amino acids by estradiol also required the presence of Na+. Uptakes of l-valine and l-phenylalanine, which were not estradiol-sensitive, were somewhat greater in the absence of sodium than in its presence. The uptake of α-aminoisobutyric acid by the uterus increased regularly as the buffer Na+ level was raised from 0 to 143 meq per liter. A Na+ level of 203 meq per liter gave even greater uptake at α-aminoisobutyric acid levels around 1 mm, but it inhibited uptake at higher levels of the amino acid, when compared with a buffer of the same tonicity containing 143 meq per liter of Na+. Reducing the buffer [Na+] from 143 to 4 meq per liter led to an approximately 6-fold increase in the Km of uptake of α-aminoisobutyric acid in both the normal and estradiol-primed tissues. The Vmax values were increased slightly. Decreasing the buffer [Na+] led to these same changes in uteri that had been preincubated for 3 hours in normal medium before uptake was measured. Stimulation of α-aminoisobutyric acid uptake by estradiol became greater as the buffer [Na+] was elevated from 4 to 203 meq per liter. At a normal buffer Na+ level of 143 meq per liter, α-aminoisobutyric acid uptake was inhibited progressively as the level of ouabain was increased over the range 0.02 to 0.2 mm. However, the ouabain produced less inhibition at a lower Na+ level, and greater inhibition at a higher Na+ level. Uptake by estradiol-primed tissues was more sensitive to ouabain inhibition than was uptake by control tissues. The interrelationships between the actions of estradiol and Na+ in transport of α-aminoisobutyric acid in the uterus are discussed in terms of an hypothesis that is consistent with the present evidence.

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