SIMULTANEOUS INFUSION OF PROSTAGLANDIN E2 ANTAGONIZES THE LUTEOLYTIC ACTION OF PROSTAGLANDIN F2α IN VIVO

1977 ◽  
Vol 72 (3) ◽  
pp. 379-383 ◽  
Author(s):  
K. M. HENDERSON ◽  
R. J. SCARAMUZZI ◽  
D. T. BAIRD

SUMMARY Corpora lutea of ewes bearing ovarian autotransplants were infused for 4 h with prostaglandin F2α (PGF2α) (10 μg/h), PGF2α + PGE2 (10 μg/h of each), PGE2 (10 μg/h) or saline on day 10 of the cycle. Ovarian venous blood obtained before, during, and up to 12 h after the infusion period, was assayed for progesterone. Prostaglandin F2α produced an immediate, rapid and sustained decline in progesterone secretion, but infusion of PGE2 together with PGF2α prevented the decline until after the infusion. Progesterone secretion was unaffected by infusion of PGE2 alone. Oestrous behaviour was observed in four out of seven animals infused with PGF2α but in only one out of six infused with PGF2α + PGE2. None of the animals infused with PGE2 alone or saline only came into heat.

1975 ◽  
Vol 67 (1) ◽  
pp. 81-88 ◽  
Author(s):  
N. L. POYSER ◽  
E. W. HORTON

SUMMARY Five guinea-pigs actively immunized against a prostaglandin F2α(PGF2α)–bovine serum albumin conjugate showed elongated oestrous cycles. During these, corpora lutea were maintained in a functional secretory state as indicated by plasma progesterone levels. The results are compatible with the view that the PGF2α antibodies neutralized the PGF2α released from the uterus and thus prevented its normal luteolytic effect. Similar patterns of progesterone secretion were observed in two hysterectomized animals and in two animals with intra-uterine implants of indomethacin.


1976 ◽  
Vol 69 (2) ◽  
pp. 275-286 ◽  
Author(s):  
D. T. BAIRD ◽  
R. B. LAND ◽  
R. J. SCARAMUZZI ◽  
A. G. WHEELER

SUMMARY The concentrations of oestradiol, androstenedione, progesterone and prostaglandin F2α (PGF2α) were measured in utero-ovarian venous blood collected throughout six oestrous cycles in two ewes with utero-ovarian autotransplants. The secretion of oestradiol was closely correlated with that of androstenedione (r = 0·67, P < 0·001) indicating a common origin from the Graafian follicle. The concentration of these two steroids fluctuated at random throughout the luteal phase with the maximum secretion occurring about 2 days before the onset of oestrus. Functional regression of the corpus luteum, as indicated by a fall in the secretion of progesterone, began on day 12 or day 13, i.e. about 4 days before the onset of oestrus. In five of the six cycles the first significant rise in the secretion of PGF2α occurred on days 12–14 at the time of decline of progesterone secretion, although the release of PGF2α was maximal on the day before the onset of oestrus. There was very little release of PGF2α from the uterus before day 12. The temporal relationship of these events suggests that the uterus will only release PGF2α after it has been primed for 7–10 days with progesterone. The initiation of luteal regression is independent of secretion of oestradiol by the pre-ovulatory follicle which may, however, stimulate the further release of PGF2α responsible for irreversible structural luteolysis on the day of pro-oestrus.


1987 ◽  
Vol 114 (2) ◽  
pp. 231-239 ◽  
Author(s):  
J. P. Hearn ◽  
G. E. Webley

ABSTRACT The interaction between luteotrophic and luteolytic agents in controlling progesterone production by the marmoset corpus luteum in the late luteal phase/early pregnancy was investigated at the local level in vivo using a perfusion cannula system. Perfusion of the prostaglandin F2α(PGF2α) analogue, cloprostenol (0·5 μg/ml), resulted in an immediate fall in progesterone production. This response was not sustained in two out of five corpora lutea but pregnancy was terminated in all animals exposed to PGF2α. Perfusion of human chorionic gonadotrophin (hCG) (4 μg/ml) alone significantly stimulated progesterone secretion but there was no response to hCG when the corpus luteum had previously been perfused with PGF2α. Perfusion with hCG together with PGF2α prevented a fall in progesterone secretion. The results suggest that the luteolytic action of PGF2α in the marmoset may be to prevent luteotrophic support of the corpus luteum. Melatonin (860 pmol/l), perfused either with PGF2α or after PGF2α, stimulated progesterone production. The ability of melatonin to influence progesterone production by the primate corpus luteum may therefore be by both a direct luteotrophic action and the prevention of luteolysis. Application of the perfusion system in order to investigate the ability of deglycosylated hCG to antagonize the action of hCG at the corpus luteum showed the necessity of testing pure preparations of hormones. J. Endocr. (1987) 114, 231–239


1972 ◽  
Vol 53 (2) ◽  
pp. 201-213 ◽  
Author(s):  
A. P. LABHSETWAR

SUMMARY In an attempt to characterize the endocrine profile of prostaglandin F2α (PGF2α) in relation to the female reproductive system, the compound (racemic form) was administered to hamsters and rats in various reproductive states. The prostaglandin terminated pregnancy when given once a day either subcutaneously (50 μg/hamster) or orally (1·5–2 mg/hamster) from Days 4 to 6 of pregnancy inclusive, or as a single subcutaneous injection (50 μg/animal) on Day 4. In the rat, higher (500 μg/injection) and more frequent (twice daily) s.c. injections were required to get even foetal resorption. Concomitant administration of progesterone (4 mg/animal) in either species protected pregnancy. Prostaglandin F2α terminated pregnancy without interfering with the Pontamine blue reaction, suggesting that its antifertility effects were not mediated by inhibition of implantation. In both hamsters and rats the prostaglandin markedly reduced the size of deciduomata which could be restored to normal by administration of progesterone. Prostaglandin F2α delayed passage of zygotes through the Fallopian tubes in a proportion of rats but failed to accelerate egg transport in rats and hamsters. Furthermore, it caused a marked histological degeneration of the corpora lutea and induced formation of a fresh set of corpora lutea in pseudopregnant, pregnant and pseudopregnant—hysterectomized hamsters. These deleterious effects of prostaglandin were accompanied, in hamsters, by the appearance of freshly ovulated tubal ova. Most of the endocrine effects of PGF2α observed in this study can be accounted for by its luteolytic property.


2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Giulia Collodel ◽  
Elena Moretti ◽  
Mariangela Longini ◽  
Nicola Antonio Pascarelli ◽  
Cinzia Signorini

Polyunsaturated fatty acid damages lead to alterations in sperm function. This study aimed to investigate the involvement of F2-isoprostanes (F2-IsoPs), oxidized lipid products from arachidonic acid, in sperm quality impairment. For this purpose, F2-IsoP levels in semen and F2-IsoP localization in spermatozoa were explored in infertile subjects affected by idiopathic infertility or varicocele, as well as in fertile men. As compared to fertile men, in the idiopathic infertility and varicocele groups, sperm concentration, motility, morphology, viability, and fertility index were significantly lower and the mean scores concerning sperm apoptosis, necrosis, and immaturity were significantly higher. The idiopathic infertile group showed a reduction in sperm motility and fertility index, as well as an increase of apoptosis and necrosis percentages, in comparison to the varicocele group. The varicocele group showed the highest levels of F2-IsoPs, a significant increase of sperm immaturity, and a significant correlation between F2-IsoP levels and sperm immaturity. 8-Iso Prostaglandin F2α, biomarker of in vivo F2-IsoP, was clearly localized in sperm midpiece and cytoplasmic residues. Data show that F2-IsoP formation is relevant in semen and sperm from infertile patients with varicocele and high percentage of immaturity, suggesting that a correct fatty acid integrity is needed for sperm maturation.


1987 ◽  
Vol 116 (3) ◽  
pp. 405-412 ◽  
Author(s):  
Martina Hoedemaker ◽  
Kirsten Grunert ◽  
D. H. A. Maas ◽  
E. Grunert

Abstract. Tissue slices from bovine corpus luteum from Days 12 or 13 of the oestrous cycle were super-fused for 8 h, and the progesterone secretion under the influence of prostaglandin F2α (PGF2α) and/or LH was measured. PGF2α at concentrations of 0.28 to 2800 nmol/l medium did not affect the basal progesterone secretion, whereas higher doses (7000 to 28 000 nmol/l) induced a slight increase in hormone secretion. LH, 3.4 nmol/l, caused an increase in the progesterone concentration in superfusates which exceeded the control levels (P < 0.01). This luteotropic effect of LH was not influenced by simultaneous addition of 28 to 2800 nmol/l PGF2α. PGF2α, 2800 nmol/l, did not inhibit progesterone secretion, when administered together with 0.034 to 34 nmol LH/l. Pre-superfusion with 2800 nmol/l PGF2α had no effect on the LH-stimulated increase in progesterone secretion. It is concluded that in cattle, a direct cellular effect of PGF2α, antagonizing the luteotropic function of LH, may be of less importance than other possible direct and indirect PGF2α actions.


1976 ◽  
Vol 68 (3) ◽  
pp. 445-451 ◽  
Author(s):  
F. R. BLATCHLEY ◽  
B. T. DONOVAN ◽  
N. L. POYSER

SUMMARY The presence of beads in the guinea-pig uterus caused premature regression of the corpora lutea, and a corresponding decrease in utero-ovarian venous plasma levels of progesterone, by days 9–10 of the oestrous cycle. If the beads were placed in one horn only, premature luteal regression occurred only in the adjacent ovary. Induced luteal regression was preceded by an increased release of prostaglandin F2α (PGF2α) from the uterine horns which contained the beads. Oestradiol benzoate treatment of guinea-pigs carrying beads in one uterine horn overcame the unilateral effect and resulted in premature luteal regression in both ovaries. This was also associated with the early release of PGF2α from both uterine horns, though a difference in the timing of the release was apparent between the bead-containing (experimental) and control horns.


1984 ◽  
Vol 105 (2) ◽  
pp. 258-265 ◽  
Author(s):  
P. A. Torjesen ◽  
A. Aakvaag

Abstract. Superluteinized rats were injected with the prostaglandin F2α (PGF2α) analogue cloprostenol to induce luteolysis. The treatment decreased progesterone production of ovarian homogenates from 8.9 ± 0.5 to 4.0 ± 0.7 nmol/ovary/10 min (mean ± sem) within 40 min. tochondrial fractions isolated from control and cloprostenol treated animals produced 4.7 ± 0.4 and 2.8 ± 0.3 nmol progesterone/ovary/10 min, respectively. Thus, the PGF2α analogue treatment significantly reduced mitochondrial progesterone production. Addition of the 15 000 × g supernatant fraction did not influence the progesterone production rates of the mitochondrial fraction. The basal progesterone secretion from quartered ovaries decreased from 1.50 ± 0.15 to 0.38 ± 0.05 nmol/ovary during the initial 15 min of incubation following cloprostenol administration. hCG and N6,O2'-dibutyryladenosine 3':5'-cyclic monophosphate (DBC) stimulated the progesterone secretion from quartered ovaries, but the response was delayed in ovaries obtained from cloprostenol treated animals. Although the response was delayed, the progesterone secretion following cloprostenol treatment was re-activated with cAMP either directly or via hCG. The increment in progesterone secretion above unstimulated controls in response to DBC was not influenced by the cloprostenol treatment while the increment caused by hCG was decreased. Our data suggest that: 1) PGF2α deactivates mitochondrial progesterone production, 2) this deactivation may be overcome by cAMP, and 3) PGF2α decreases gonadotrophin responsive adenylyl cyclase.


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