Hexose Transport and Blood Flow Rate in the Uterus: Effects of Estradiol, Puromycin and Actinomycin D1

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Abstract
Estradiol increased net intracellular uptake of the nonmetabolizable sugar, 3-0-methyl (14c)-glucose, from a control distribution of 59% to a distri-bution of 75% of the uterine volume and over the sucrose space (59%) in estrogen-treated rats. Puromycin given alone or with estradiol depressed methyl glucose distribution below control levels (to 53%); puromycin also prevented estrogen-induced water uptake and increase in blood flow rate. All animals receiving puromycin exhibited toxic signs, including large amounts of abdominal fluid, a contracted extra-cellular compartment (40% sucrose space in uterus) and an increase of 17% in hematocrit. Prior adrenalectomy did not alter these results, except that hematocrit increased 47% above normal. Estradiol and puromycin did not affect methyl glucose distribution in skeletal muscle, but puromycin tended to depress sucrose space. Actinomycin D prevented the increase in uterine methyl glucose distribution (but not water uptake) due to estradiol but did not affect this estrogen response after adrenalectomy; the suppressive action of actinomycin D therefdre was secondary to the estrogen-antagonizing effects of adrenal gluco-cortical hormones. Conclusions: early estrogen-stimulated hexose transport and hydration in the uterus are independent of synthesis of new messenger RNA but may be dependent upon induced or otherwise increased synthesis of one or more proteins. However, the inhibitory effects of puromycin may have resulted, in part at least, from the drug''s deleterious side-effects, including depression of uterine blood flow. Estradiol produced a significant increase in uterine blood flow rate within 30 min. of hormone injection (controls: 0.27, exptl.: 0.36 ml/min/g) and a linear increase thereafter to the 4th hr. (to approxi-mately 0.71). Flow rate in liver was not affected by estradiol. These early responses are discussed in relation to current theories of estrogen action at cellular and molecular levels.
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