Hexose Transport and Blood Flow Rate in the Uterus: Effects of Estradiol, Puromycin and Actinomycin D<sup>1</sup>

Spaziani, Eugene; Suddick, Richard P.

doi:10.1210/endo-81-2-205

Cited by 38 publications

(17 citation statements)

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“…The suitability of this method for measuring changes in uterine blood flow was illustrated in Exp. 1: oestrogen treatment increased uterine blood flow 5-fold in ovariectomized animals, similar to the results obtained in rats using rubidium (Spaziani, & Suddick, 1967). The proportion of cardiac output perfusing the uterus of the ovariectomized, oestradiol-treated mouse in the present study (017 + 003%) is similar to that in non-pregnant rats (012 + 001%) (Ahokas et al, 1983).…”

Section: Resultssupporting

confidence: 86%

Uterine blood flow during the development and regression of the decidual cell reaction in ovariectomized, steroid-treated mice

Edwards¹,

Milligan²

1987

Reproduction

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Summary. Uterine blood flow was assessed in mice by measuring organ uptake of intravenously injected [14C]butanol. In ovariectomized mice, injection of 100 ng oestradiol\x=req-\ 17\g=b\ increased blood flow 5-fold over that of untreated controls. The injection of oestradiol-17\g=b\ in progesterone-treated mice also increased uterine blood flow at the time of maximal sensitivity to a decidual stimulus, but not 4 days later. Absolute values of blood flow increased during development of the decidual cell reaction in proportion to the increase in uterine weight, reaching maximal values 96 h after decidual induction. When progesterone injections were stopped 72 h after decidual induction, a rapid decrease in absolute and relative blood flow values preceded the decrease in uterine weight. This decrease in uterine blood flow occurred within 12 h of removing a subcutaneous implant containing progesterone. These results are consistent with the view that increased uterine blood flow during decidual development may be necessary to support the rapid increase in uterine weight at implantation and the subsequent decrease in both relative and absolute uterine blood flow on withdrawal of progesterone may promote decidual regression in the mouse.

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Section: Resultssupporting

confidence: 86%

Uterine blood flow during the development and regression of the decidual cell reaction in ovariectomized, steroid-treated mice

Edwards¹,

Milligan²

1987

Reproduction

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“…The ability of the estrogen (and progesterone) produced by the ovary to regulate the synthesis of prostaglandins by the uterus in a directional and cyclic manner is consistent with the unique roles played by PGEs and PGF2a in the reproductive processes. One of the initial effects of estrogen upon the uterus is to induce a rapid hyperemia (25). There is much evidence to strate precursor acids.…”

Section: Changes In Uterine Prostaglandin Levels During the Estrus Cyclementioning

confidence: 99%

Estrogen-directed synthesis of specific prostaglandins in uterus.

Ham¹,

Cirillo²,

Zanetti³

et al. 1975

Proc. Natl. Acad. Sci. U.S.A.

128

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Endogenous uterine prostaglandin levels were monitored in the cycling rat and prostaglandins of the F-type were found to rise at proestrus when estrogen levels have been shown to be maximal. Evidence that this is an estrogen-induced event is furnished by the finding that estradiol-17fl caused a similar rise in prostaglandin F levels in uteri of ovariectomized rats, an action blocked by coadministration of progesterone. Examination of in vitro prostaglandin synthetase by uterine microsomal fractions from cycling rats and estrogen-treated ovariectomized rats revealed that the action of estrogen to control prostaglandin synthesis in a directional manner is accomplished, at least in part, by regulation of the prostaglandin synthetase complex, resulting in a patterned alteration in the ratio of prostaglandin F to prostaglandin E. These results demonstrate that prostaglandins are involved in the expression of estrogen action in the rat uterus.Estrogen administration has been shown to effect the release of prostaglandin F2a (PGF2a) into uterine fluids of the guinea pig (1) and monkey (2). This prostaglandin, which has a potent contractile effect on the isolated uterus, has been identified in sheep as the luteolytic agent produced by the uterus which subsequently acts on the ovary to bring about luteal regression (3). Estrogen administration has also been shown to be associated with uterine hyperemia (4). Such hyperemia has been related to elevations in prostaglandin E (PGE) levels (5, 6). These findings, plus new data demonstrating the existence of receptors unique to PGE1 and PGF2, in the uterus (7) and corpus luteum (8, 9), pose the possibility that PGEs and PGF2a,, produced in the uterus as a consequence of estrogen action, play distinctly different roles in the reproductive processes.Recently, the action of estrogen on the uterus of the ovariectomized rat has been shown to be associated with a rise in guanosine 3': 5'-cyclic monophosphate (cyclic GMP) (10), an observation strengthened by the finding that cyclic GMP is maximal in the normal cycling rat at proestrus (10), a time when estrogen levels reach their peak value (11). Although there is evidence that the contractile effect of PGF2a on the uterus (N. D. Goldberg et al., personal communication and ref. 21) as well as on the canine saphenous and lung veins is associated with a rise in cyclic GMP levels (12, 13), estrogen itself exhibits no such acute contractile action on the isolated uterus. Thus, in view of the demonstrated ability of estrogen to trigger the production of both cyclic GMP and PGF by this organ, we were prompted to examine these events in more detail.Emphasis was placed on the estrogen-regulated biosynthesis of prostaglandins E and F, as well as the interrelationships between these prostaglandins and adenosine 3': 5'-cyclic monophosphate (cyclic AMP) and cyclic GMP. The results of these studies are the substance of this report. Female Charles River rats (150-250 g) were used throughout these studies. The stages of their estrus cycle wer...

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“…Estrogen injection to spayed rats rapidly enhanced the phospholipid synthesis and it was found that 3-0-methylglucose transport in vivo and in vitro into uterus increased in the early phase of hormone admini stration (1,2,12). It is an established fact that phospholipid in tissues is an important component of membrane which is composed mainly of lipids and protein, even though the basic arrangements of these two components are not yet clear.…”

Section: Resultsmentioning

confidence: 99%

Role of Phospholipid in the Effect of Estradiol on Sugar Transport in Rat Uterus

Kuroda¹,

Aizawa²

1972

Jpn.J.Pharmacol

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In 1961, one of the authors (1) demonstrated that estrogen stimulated the biosynthesis of phospholipids in the ovariectomized rat uterus and phospholipid metabolism constitutes an unusually sensitive indicator of early estrogen action. Recently, Roskoski and Steiner reported that estrogen injection increases the initial rate of 3-0-methylglucose transport into uterine cells and this transport takes place by means of a specific mobile carrier trans port system (2).
Phospholipid is an essential component of biological membrane (3, 4) and it has been clarified that phospholipid affects various enzymic reactions (5-10). Membrane lipid is also of interest in this regard as it may play an important role in transport of a substance through cell membrane.
This present report is an investigation as to whether or not sugar transport into uterine cells, which is accelerated by estrogen administration, is affected by phospholipids in vitro. It was observed that sugar transport in the spayed rat uterus increased with the addition of phospholipid. METHODSUnless otherwise specified, Wistar strain female rats, weighing approx. 100g, were spayed the same day under ether anesthesia and maintained for 3 weeks, then subcutaneous injections of 10,eg l71 -estradiol in 0.1 ml of sesame oil or the vehicle alone. They were then sacrificed by decapitation at an indicated time. The 3-0-("C)methyl-D-glucose (16.5 mCi/mmole) and D-(l-3H)-sorbitol (6.7 Ci/mmole) were obtained from New England Nuclear Corporation. Incubation procedures carried out were similar to the method of Roskoski and Steiner (2), at the end of which time, the uterus horns were washed twice with 5 ml of Krebs-Ringer bicarbonate solution (pH 7.4). Each horn was incised longitudi nally, blotted on dry filter paper, weighed on torsion balance, and transferred to microtest tube. After tubes had been boiled for 15 min, uterine tissues were homogenized with I ml of 5 trichloroacetic acid in an all glass homogenizer and the uterine homogenates were centrifuged at 800 g for 15 min. From one-tenth to three-tenths ml aliquot of the clear supernatant was completely evaporated in a counting vial. The residue was dissolved in 0.1 ml of distilled water and five ml of scientillation solution (4 g of 2,5-diphenyloxazole plus 0.1 g of 1,4-bis-2-(methyl-5-phenyl-oxazolyl) benzene per liter of toluene plus 300 ml

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

Cited by 38 publications

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Uterine blood flow during the development and regression of the decidual cell reaction in ovariectomized, steroid-treated mice

Uterine blood flow during the development and regression of the decidual cell reaction in ovariectomized, steroid-treated mice

Estrogen-directed synthesis of specific prostaglandins in uterus.

Role of Phospholipid in the Effect of Estradiol on Sugar Transport in Rat Uterus

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

Cited by 38 publications

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Uterine blood flow during the development and regression of the decidual cell reaction in ovariectomized, steroid-treated mice

Uterine blood flow during the development and regression of the decidual cell reaction in ovariectomized, steroid-treated mice

Estrogen-directed synthesis of specific prostaglandins in uterus.

Role of Phospholipid in the Effect of Estradiol on Sugar Transport in Rat Uterus

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