The acute effect of placentectomy and hysterectomy on peripheral plasma progesterone levels and ovarian progesterone secretion in the pregnant rat

1983 ◽  
Vol 98 (1) ◽  
pp. 71-77 ◽  
Author(s):  
J. K. Olynyk ◽  
N. W. Bruce ◽  
B. J. Waddell

The role of placental luteotrophins in modulating plasma progesterone concentrations and ovarian progesterone secretion was examined in 16-day pregnant rats. In an initial experiment rats were placentectomized and their plasma progesterone concentrations monitored for 24 h; the rats were conscious within 30 min of placentectomy. Relative to control values, progesterone concentrations fell significantly within 0·5 h. A venous outflow technique was then used to monitor rates of progesterone secretion from ovaries of hysterectomized and control rats maintained under anaesthesia. Hysterectomy had no apparent effect on either progesterone secretion or plasma progesterone concentrations for at least 2 h. A final experiment was carried out to compare the effects of hysterectomy on plasma progesterone concentrations in conscious rats with those of placentectomized rats of the first experiment. Progesterone concentrations did not change significantly in hysterectomized rats for 4 h but fell to very low values by 24 h. These results suggest that placental luteotrophins do not have an acute, direct role in the control of plasma progesterone levels but are needed to maintain progesterone secretion in the longer term and possibly inhibit uterine luteolysin release.

1982 ◽  
Vol 94 (1) ◽  
pp. 61-67 ◽  
Author(s):  
B. J. Waddell ◽  
N. W. Bruce ◽  
J. K. Olynyk

We have sought to determine whether the rate of ovarian progesterone secretion in pregnant rats is inversely related to the arterial plasma progesterone concentrations. For this purpose, rates of ovarian progesterone secretion were measured on day 16 of pregnancy in seven progesterone-treated and eight untreated rats. Treated rats received once-daily s.c. injections of 63·6 μmol progesterone in peanut oil on days 13 to 16. In a separate experiment, this treatment was found to produce a relatively stable fivefold increase in plasma progesterone concentrations. The rate of ovarian blood flow was increased in treated animals (mean ± s.e.m.; treated, 0·63± 0·08 ml/min; untreated, 0·43± 0·08 ml/min) but the progesterone secretion rate was unchanged (treated, 1·13 ± 0·20 μmol/day per ovary; untreated, 1·05 ± 0·15 μmol/day per ovary). The stability of the progesterone secretion rate in the face of a fivefold increase in plasma progesterone concentration implies a lack of negative feedback from progesterone in plasma in the regulation of ovarian progesterone secretion.


1981 ◽  
Vol 90 (2) ◽  
pp. 179-191 ◽  
Author(s):  
S. HENDRICKS ◽  
C. A. BLAKE

The effects of varying amounts of copulatory stimulation on patterns of plasma concentrations of prolactin and progesterone were evaluated in 3- and 12-month-old female rats. The 12-month-old group included rats which still exhibited oestrous cycles and rats in persistent vaginal oestrus (PVO). The extent of copulatory stimulation was defined by the number of intromissions received during mating: ≤5,15 or > 50. Blood samples were drawn over the 8 days after mating through a cannula inserted into the right external jugular vein. Plasma from the samples was assayed for prolactin and progesterone. In aged but still cyclic rats, pregnancy rates were positively correlated with the number of intromissions received during mating. Only one rat in PVO became pregnant. All animals which became pregnant and rats in PVO which, after mating, exhibited a disruption of the pattern of PVO, showed the nocturnal surge of plasma prolactin characteristic of pregnant and pseudopregnant rats. While these surges persisted until day 8 after mating in pregnant animals, they were absent by this time in the rats in PVO. Prolactin surges were present in some but not all of the aged rats which did not become pregnant. Progesterone concentrations were raised in all pregnant animals except the one pregnant rat in PVO and, while not related to the number of intromissions, concentrations were higher 8 days after mating in young compared with those in aged pregnant rats. Plasma progesterone was low in rats in PVO regardless of disruption of the pattern of PVO. We have concluded that the failure of limited copulatory stimulation to induce pregnancy in older rats results, at least in part, from its failure to initiate nocturnal prolactin surges. Nevertheless, our data suggest that matings which are not experimentally limited should provide ample stimulation to establish such surges. Although reduced plasma concentrations of prolactin and progesterone at pro-oestrus and reduced plasma progesterone through part of gestation may contribute to decreasing fertility in aged rats, other unidentified factors appear to be involved in mediating the capacity of extensive copulatory stimulation to induce pregnancy in these animals.


1972 ◽  
Vol 53 (1) ◽  
pp. 31-35 ◽  
Author(s):  
K. BROWN-GRANT ◽  
C. S. CORKER ◽  
F. NAFTOLIN

SUMMARY Plasma luteinizing hormone (LH) concentrations were already lower on Day 2 of pregnancy than at the same time after the preceding ovulation in the non-pregnant rat, and fell progressively up to Day 16 of pregnancy. No evidence was obtained of any increase at the time when the ovulatory surge of LH would have occurred if the animal had not become pregnant. Pituitary LH concentration was lower in mated rats on the morning of Day 0 of pregnancy than in unmated controls on the morning of the day of oestrus. Subsequently it increased slowly to reach a level higher than at any stage of the oestrous cycle by Day 8 of pregnancy and remained high until at least Day 16 of pregnancy. Peripheral plasma oestradiol concentration increased late on Day 2 of pregnancy and was still raised on Day 4 but was never more than about one fourth of the peak concentration seen on the morning of prooestrus during the oestrous cycle. There were similar changes in plasma LH and oestradiol concentrations in the 48 h after a single injection of 2·5mg progesterone on the morning of the day of dioestrus, a procedure that delays ovulation by 1 or 2 days. Administration of a synthetic progestational compound (medroxyprogesterone acetate) to pregnant rats delayed blastocyst implantation and the delay was associated with a marked decrease in peripheral plasma LH to levels below those of normal pregnancy.


1988 ◽  
Vol 118 (1) ◽  
pp. 59-68 ◽  
Author(s):  
L. V. DePaolo

ABSTRACT Epostane, an inhibitor of 3β-hydroxysteroid dehydrogenase, was administered orally to pro-oestrous rats to evaluate further a possible role for preovulatory progesterone secretion in eliciting surges of LH and FSH. Whereas a dose of 10 mg epostane/kg had essentially no effects on preovulatory gonadotrophin surges and ovulation, 200 mg epostane/kg markedly attenuated LH and FSH surges and blocked ovulation. A dose of 50 mg epostane/kg exerted effects on LH and FSH surges and ovulation intermediate between those of doses of 10 and 200 mg/kg. Plasma concentrations of progesterone were significantly lower in all anovulatory epostane-treated rats at 18.00 and 22.00 h on pro-oestrus than those measured in vehicle-treated rats. Concurrent injection of 2 mg progesterone in rats given 200 mg epostane/kg restored gonadotrophin surges to normal, but consistently failed to reverse the inhibitory effects of epostane on ovulation. Peak plasma progesterone levels produced by the progesterone injections were eight- to tenfold higher than the highest levels measured in vehicle-treated rats during the afternoon of pro-oestrus. Insertion of progesterone capsules was less effective than injections of progesterone in restoring gonadotrophin surges to normal, even though peak plasma progesterone concentrations achieved after insertion of two 20 mm long progesterone capsules were double the peak progesterone concentrations measured in control rats. Nevertheless, taken together with recent reports showing attenuation of preovulatory gonadotrophin surges by the progesterone antagonist RU 486 (17β-hydroxy-11β-[4-dimethyl-aminophenyl]-17α-[prop-1-ynl]estra-4,9-diene-3-one), the present results provide support for a role of preovulatory progesterone secretion in enhancing oestrogen-dependent LH/FSH surges on pro-oestrus. J. Endocr. (1988) 118, 59–68


1983 ◽  
Vol 210 (3) ◽  
pp. 761-767 ◽  
Author(s):  
G E Bunce ◽  
G R Wilson ◽  
C F Mills ◽  
A Klopper

1. Pregnant rats were fed either low (less than 1 p.p.m.) Zn or control (40 p.p.m. Zn) diets from day 10 of gestation. They were killed at intervals during the last 96 h preceding the normal time for onset of parturition, and differences in plasma progesterone, oestradiol-17 beta and ovarian 20 alpha-hydroxysteroid dehydrogenase were assessed. 2. Gestation was prolonged in Zn-deficient rats. 3. Although the preparturient decline in plasma progesterone began at the same time in all groups, at term, plasma progesterone concentration in Zn-deficient rats remained significantly higher than in normal females. 4. Induction of ovarian 20 alpha-hydroxysteroid dehydrogenase activity was delayed by about 8 h by Zn deficiency. This delay was not observed if prostaglandin F2 alpha was injected previously. 5. The results suggest a Zn-dependent step(s) in uterine synthesis and/or release of prostanoids.


1985 ◽  
Vol 63 (2) ◽  
pp. 136-142 ◽  
Author(s):  
Graham Jenkin ◽  
Geoffrey D. Thorburn

The role of progesterone in the initiation of parturition in the sheep is unclear. Whether a decrease in plasma progesterone is the essential prerequisite for the initiation of parturition or whether other factors also maintain uterine quiescence until delivery is not known. The effect of withdrawal of progesterone on the initiation of parturition has been investigated by intravenous administration of trilostane, a 3β-hydroxysteroid dehydrogenase Δ5−4 isomerase inhibitor, to late pregnant sheep. Twenty-five or 100 mg trilostane caused a precipitous decrease in plasma progesterone to about 30% of preinjection levels. Progesterone remained depressed for up to 7 days after treatment. 13,14-Dihydro-15-keto-prostaglandin F2α (PGFM) became elevated between 7 and 36 h after trilostane injection but gradually returned to preinjection levels during the subsequent 36 h, at a time when plasma progesterone was still depressed. Four of 11 animals treated with 100 or 200 mg trilostane aborted prematurely at a time when plasma PGFM was maximal and plasma progesterone minimal. There were no consistent changes in plasma estradiol-17β or ovine placental lactogen concentrations after treatment with trilostane. It is suggested that a decrease in plasma progesterone will cause a transient increase in plasma PGFM concentrations which can lead to the premature initiation of parturition. In some instances the myometrium does not appear to respond to the elevated PGFM concentrations even when the estrogen:progesterone ratio is elevated by a decrease in plasma progesterone.


2016 ◽  
Vol 27 (9) ◽  
pp. 1420-1430 ◽  
Author(s):  
David W. Scott ◽  
Caitlin E. Tolbert ◽  
Keith Burridge

Junctional adhesion molecule A (JAM-A) is a broadly expressed adhesion molecule that regulates cell–cell contacts and facilitates leukocyte transendothelial migration. The latter occurs through interactions with the integrin LFA-1. Although we understand much about JAM-A, little is known regarding the protein’s role in mechanotransduction or as a modulator of RhoA signaling. We found that tension imposed on JAM-A activates RhoA, which leads to increased cell stiffness. Activation of RhoA in this system depends on PI3K-mediated activation of GEF-H1 and p115 RhoGEF. These two GEFs are further regulated by FAK/ERK and Src family kinases, respectively. Finally, we show that phosphorylation of JAM-A at Ser-284 is required for RhoA activation in response to tension. These data demonstrate a direct role of JAM-A in mechanosignaling and control of RhoA and implicate Src family kinases in the regulation of p115 RhoGEF.


1989 ◽  
Vol 257 (4) ◽  
pp. R866-R871 ◽  
Author(s):  
M. S. Paller ◽  
G. Gregorini ◽  
T. F. Ferris

During pregnancy the pressor response to vasoconstrictor substances such as angiotensin II (ANG II) is diminished, and renal, uterine, and vascular prostaglandin (PG) production may increase. However, little is known about the factors that alter vascular reactivity or stimulate PG synthesis during pregnancy. To ascertain whether these factors are of maternal or fetal-placental origin, we studied vascular reactivity and urinary PGE excretion in pseudopregnant rats. Pseudopregnant rats had plasma progesterone and weight gain similar to that observed in pregnant rats. Urinary PG excretion in nonpregnant rats was approximately 70 ng/24 h and remained constant during a 12-day observation. In contrast, urinary PG excretion in both pregnant and in pseudopregnant rats rose to levels approximately twice control within 4-6 days. The pressor response to ANG II was diminished in pseudopregnant rats compared with nonpregnant rats. When the PG synthesis inhibitor meclofenamate was given there was no change in the pressor response to ANG II in nonpregnant animals, but in pseudopregnant animals meclofenamate produced a significant increase in the pressor response to ANG II. The pressor response to norepinephrine and arginine vasopressin (AVP) was not diminished in pseudopregnant animals, and meclofenamate did not increase the pressor response to these agents. Therefore, a developing fetus and placenta is not necessary for the decrease in pressor response to ANG II nor for the early increase in urinary PGE excretion. Like in pregnancy, the pressor response to ANG II was increased after meclofenamate in pseudopregnancy. Increased PG production may, therefore, be partly responsible for the decrease in pressor responsiveness to ANG II. However, pseudopregnancy, unlike pregnancy, did not affect pressor responsiveness to norepinephrine or AVP. Both maternal and fetal-placental factors seem required for the reduction in responsiveness to norepinephrine and AVP in pregnancy.


1987 ◽  
Vol 112 (1) ◽  
pp. 15-21 ◽  
Author(s):  
K. J. Bailey

ABSTRACT The patterns of peripheral progesterone concentrations were investigated in a number of murine models on a 13 h light: 11 h darkness lighting regime. The pattern in the intact mouse at dioestrus was compared with that in the ovariectomized mouse. A diurnal pattern was recorded in both, maxima occurring around the end of the light period; no conspicuous nadir was recorded, levels of progesterone remaining relatively constant over a 14-h period. Adrenalectomized mice displayed no such rhythm, indicating that the adrenal is responsible for any diurnal rhythm in peripheral plasma progesterone concentrations at dioestrus. At pro-oestrus in intact animals a similar rhythm was observed, but the maximum levels of progesterone were approximately five times greater than at dioestrus and, moreover, persisted in adrenalectomized mice, indicating that the rhythm of adrenal secretion of progesterone is masked by ovarian secretion. Ovariectomized mice with implants of oestradiol-17β displayed a similar rhythm to that of intact mice at dioestrus, but had significantly higher plasma progesterone levels around the time of the maxima although not over the total 24-h period. An s.c. injection of oestradiol benzoate superimposed on oestrogen levels produced by implants had no significant effect on plasma progesterone levels. Also at pro-oestrus the pattern of peripheral LH concentration was investigated in both the intact and the adrenalectomized mouse. For both, maxima were recorded just before darkness, at 19.00 h, in advance of the progesterone surge. In adrenalectomized mice this surge at 19.00 h was attenuated. The possible role of adrenal progesterone in ovulation and the mechanisms by which endogenous oestrogens might enhance adrenal progesterone output are considered. J. Endocr. (1987) 112, 15–21


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