Changes in endogenous prostaglandin levels during D-galactosamine-induced liver injury

The role of prostaglandins (PGs) in liver injury induced by D-galactosamine was investigated in the rat. The contents of PGD2 and PGF2 alpha in the liver were significantly increased from 3 h and 24 h after the D-galactosamine administration, respectively, but that of PGE2 was not significantly changed. Administration of 16,16-dimethyl PGE2, a long acting derivative of PGE2, or indomethacin, but not 16,16-dimethyl PGF2 alpha, a long acting derivative of PGF2 alpha, significantly depressed the increase in the serum transaminase activities induced by D-galactosamine. The protective effect of indomethacin was not disturbed by the 16, 16-dimethyl PGF2 alpha administration. These results indicate that PGE2 has a cytoprotective effect against the D-galactosamine induced liver injury and suggest that the protective effect of indomethacin is ascribable to its suppression of synthesis of PGs other than PGE2 or PGF2 alpha, e.g., PGD2.     

Effects of superovulation, arachidonic acid or endometrium on release of prostaglandins and synthesis of proteins by bovine trophoblast

This study was conducted in vitro to examine factors that may regulate prostaglandin release by bovine trophoblast and endometrial slices. Trophoblastic tissues and endometrial slices were recovered from superovulating and normally-ovulating cattle on day 16 or 20 of pregnancy and incubated for 24 h. Release of PGF2 alpha and 13,14-dihydro-15-keto-PGF2 alpha (PGFM), and incorporation of [14C]-leucine into proteins were quantified and expressed per microgram DNA, which gives a measure of cellular activity. Activity of trophoblastic tissue for synthesizing protein was decreased (P less than .05) and for releasing PGFM was increased (P less than .05) on day 20 compared to day 16 of pregnancy. Neither superovulation nor day of pregnancy altered trophoblastic activity for releasing PGF2 alpha. Superovulation increased (P less than .05) endometrial release of PGF2 alpha. Endometrial release of PGF2 alpha was less (P less than .05) on day 20 than on day 16 of pregnancy. When arachidonic acid (0, 100, 200 or 400 micrograms) was added at the start of incubation, trophoblastic release of PGF2 alpha changed (P less than .05) quadratically with dose of arachidonic acid. When arachidonic acid was added 8 h after the start of incubation, trophoblastic release of PGF2 alpha increased linearly (P less than .01) with dose of arachidonic acid. Adding arachidonic acid to incubation medium did not affect trophoblastic or endometrial protein synthesis. Endometrial slices suppressed (P less than .05) trophoblastic protein synthesis and release of PGF2 alpha. Apparently, endometrium can modulate trophoblastic release of prostaglandins and synthesis of proteins in vitro, and trophoblastic tissue from superovulated cattle 16 or 20 days pregnant can be used to study trophoblastic synthesis of prostaglandins and proteins.     

The effects of synthetic prostaglandin analogs on canine hepatic bile flow.

The synthetic prostaglandin analogs 16, 16-dimethyl PGF2 alpha and 16, 16-dimethyl PGE2 were administered to dogs with chronic biliary and gastric fistulas. The effects of 16, 16 diMePGF2 alpha and 16, 16 diMePGE2 were evaluated on bile flow and composition and bile adenosine 3', 5' monophosphate (cyclic AMP) secretion. 16, 16 diMePGF2 alpha in doses of 0.125 and 0.25 microgram-kg-min significantly increased hepatic bile flow. The choleresis was characterized by increased chloride and bicarbonate secretion. Measurement by radioimmunoassay of bile cyclic AMP concentration demonstrated no evident increase in bile cyclic AMP secretion associated with the choleresis produced by 16, 16 diMePGF2 alpha. The administration of 16, 16 diMePGE2 in a dose range 0.01 to 1.0 microgram-kg-min did not significantly alter bile flow rates or composition. Bile erythritol-14C clearance, a measure of canalicular bile flow, was significantly increased by PGF2 alpha but not by 16, 16-dimethyl PGF2 alpha, suggesting that the mechanism of action of PGF2 alpha in stimulating hepatic bile flow may be different from that involved in 16, 16-dimethyl PGF2 alpha choleresis. The results of this study indicate that the synthetic PGF2 alpha analog produces a choleretic response not mediated by adenylate cyclase and associated with increased chloride and bicarbonate secretion.     

Effect of prostaglandin E2 alpha on the hCG-stimulated progesterone production by human corpora lutea

The effect of prostaglandin PGF2 alpha on the hCG stimulated and basal progesterone production by human corpora lutea was examined in vitro. hCG (40 i.u./ml) stimulated progesterone formation in corpora lutea of early (days 16-19 of a normal 28 day cycle), mid (days 20-22) and late (days 23-27) luteal phases. This stimulation was inhibited by PGF2 alpha (10 micrograms/ml) in corpora lutea of mid and late luteal phases. PGF2 alpha alone did not show a consistent effect on basal progesterone production. The inhibition of hCG stimulated progesterone production by PGF2 alpha at times corresponding to luteolysis indicates a role for that prostaglandin in the process of luteolysis in the human corpus luteum.     

Relationship between doses of prostaglandin F2alpha and stages of the breeding season for synchronization of estrus and ovulation in ewes

Two experiments were conducted to compare estrous response to three doses (8, 16 and 24 mg) of prostaglandin F(2alpha) (PGF(2alpha)) administered by intramuscular injection to ewes between day 6 and 12 of the estrous cycle (Experiment I) and to ewes on unknown days of the estrous cycle during four different stages of the breeding season (Experiment II). In experiment I, a total of 41 ewes were treated with PGF(2alpha). The injection of 24 mg PGF(2alpha) resulted in a higher proportion of ewes exhibiting estrus (13 14 , 92.9%) within 5 days after treatment as compared to the other two doses (2 12 and 10 15 , for 8 and 16 mg PGF(2alpha), respectively). However, there was no significant difference for the proportion between 16 mg and 24 mg PGF(2alpha). In experiment II, PGF(2alpha) was given to ewes on the 3rd of February (early breeding season), the 28th of February (mid-early breeding season), the 10th of April (mid breeding season) and the 27th of May (late breeding season). These was a significant difference for the proportion of ewes exhibiting estrus between the early breeding season and the other three seasons (P < 0.05) but not for ewes ovulating. Throughout the breeding season, 16 mg PGF(2alpha) appeared to be slightly better than the other two doses (8 and 24 mg) although there was no overall difference in the estrous responses to treatment among the three doses. However, a significant difference in the proportion of ewes ovulating was found among the three doses of PGF(2alpha) (P < 0.05). Especially, 16 mg PGF(2alpha) was significantly superior to 8 mg (P < 0.01) and 24 mg (P < 0.05). It was considered that there was a complicated relationship between the doses of PGF(2alpha) and the stages of the breeding season for induction of estrus and ovulation in the ewe.     

Effects of prostaglandins, dibutyryl cAMP, LHRH, estrogens, progesterone, and potassium on output of prostaglandin F2 alpha, 13, 14-dihydro-15-keto-prostaglandin F2 alpha, hCG, estradiol, and progesterone by placental minces

In order to compare the endocrine response of placental minces to luteinizing hormone releasing hormone (LHRH) and dibutyryl cAMP (dbcAMP) and to screen for effects of potential stimulatory and inhibitory substances, the simultaneous outputs of PGF2 alpha, 13, 14-dihydro-15-keto-prostaglandin F2 alpha (PGFM), progesterone, 17 beta-estradiol, and hCG were evaluated during a 4 hour incubation in 5 placentas. The output of hCG was highest for 12-week placentas, intermediate for a 16 week placenta, and lowest for term placentas. The output of 17 beta-estradiol by 12 and 16 week placentas in the presence of 30 microM dehydroepian-drosterone sulfate (DHEAS) was greater than that by term placentas. Progesterone output was apparently independent of gestational age although some variation between 12-week placentas was demonstrated. Output of PGF2 alpha was lower in 12 and 16-week placentas than in term placentas and that of PGFM was lower in 12-week placentas than in term placentas. LHRH (100 nM) produced stimulation of PGF2 alpha output (P less than .005) and a trend toward inhibition of progesterone output (which failed to achieve statistical significance) but no stimulation of hCG under these conditions. Stimulation of the outputs of hCG (P less than .005) and PGF2 alpha (P less than .001) and inhibition of that of progesterone (P less than .005) was produced by 20 mM dbcAMP. DHEAS inhibited output of progesterone (P less than .01) and PGF2 alpha (P less than .01). There were no effects of potassium, estrogens, progesterone, or prostaglandins on output of any measured substance.     

Characterization of thymosin alpha 1 and beta 4 during the bovine estrual period: effects of elevated estradiol and progestin

At present, there is a renewed interest in thymic function and its secretions in relation to endocrine control and reproductive function. In an initial experiment, 60 crossbred heifers (18-20 mo) were detected in estrus and assigned to control or FSH superovulatory groups. On Days 7-14 of the subsequent estrous cycle, FSH was administered for 5 days and prostaglandin F2 alpha (PGF2 alpha) was administered at 48 and 60 h after the initial FSH injection. Control animals received only PGF2 alpha injections between Days 9 and 15 of the cycle. Blood samples were collected from all animals at the time of PGF2 alpha injection and every 12 h thereafter to 72 h post PGF2 alpha injection. In a subsequent experiment, 103 crossbred heifers (16-18 mo) were superovulated with FSH and synchronized to estrus with PGF2 alpha administered 60 h after the initial FSH injection. Twenty-eight of the heifers received Norgestomet implants 12 h prior to the initial PGF2 alpha injection to inhibit the LH surge. Blood samples were collected from animals at 12-h intervals until the PGF2 alpha injection and every 6 h thereafter until 108 h post PGF2 alpha treatment. Although thymosin beta 4 concentrations did change over the estrual period, no differences were noted between control and superovulatory animals in the initial experiment even though estradiol concentrations were increased tenfold from the FSH stimulated ovary. In the second experiment, thymosin beta 4 and alpha 1 increased as the estrual period progressed and decreased (p less than 0.05) subsequent to the LH surge. (ABSTRACT TRUNCATED AT 250 WORDS)     

Transport of uterine PGF2 alpha to the ovaries by systemic circulation and local lymphovenous-arterial diffusion during luteolysis in sheep.

The theory of countercurrent vascular transfer of PGF2 alpha during luteolysis was examined. In the first experiment, pulmonary clearance of PGF2 alpha was determined to re-examine whether the total amount of PGF2 alpha was degraded in the lungs after one passage. Cardiac output was measured by the Fick method and PGF2 alpha by radio-immunoassay before and after vascular lung supply, using pulmonary catheterization and the interventional radiology method in ten anaesthetized ewes on day 16 of the oestrous cycle. Cardiac output remained stable (7156 +/- 439 ml min-1). Infusion of 5 iu oxytocin resulted in an increase in plasma PGF2 alpha concentrations at 30 min in the uterine vein and the pulmonary and femoral arteries (3811 +/- 806, 224 +/- 55 and 18 +/- 4 pg ml-1, respectively). The PGF2 alpha concentrations decreased exponentially and the half-time decreases were 27 (r = 0.99), 16 (r = 0.99) and 18 (r = 0.98) min, respectively. Pulmonary clearance of PGF2 alpha was estimated at 6338 +/- 451 ml min-1. In a second experiment, an arterio-arterial gradient of plasma PGF2 alpha concentrations was analysed between the proximal and distal segments of the ovarian artery to verify whether the total amount of PGF2 alpha flowing to the ovary was from the local venous-arterial countercurrent pathway. Surgical catheterization techniques were performed on 11 ewes on day 16 of the oestrous cycle. The ovarian arterial blood flow was measured by the implantable Doppler method (8 +/- 1 ml min-1). The maximum plasma PGF2 alpha concentrations in the femoral and distal ovarian arteries were 23 +/- 6 and 42 +/- 11 pg ml-1 (P < 0.05), respectively. Plasma PGF2 alpha decreased exponentially in the femoral artery and the half-time decrease was 26 min (r = 0.98), and in the distal ovarian artery close to the ovary PGF2 alpha decreased linearly and the half-time decrease was 108 min (r = 0.96). Consequently, the arterio-arterial diffusion gradient of PGF2 alpha concentrations was extended to 3 h. These experiments showed that the PGF2 alpha flow rate in the pulmonary artery was 42.275 +/- 10.793 micrograms per 150 min (n = 10) and the systemic arterial PGF2 alpha flow rate was 5.359 +/- 1.658 micrograms per 150 min (n = 10). Therefore, 12% of the PGF2 alpha was not oxidized by the lungs. The proximal ovarian PGF2 alpha flow rate was 6.909 +/- 2.341 ng per 150 min, while the distal flow rate was 21.003 +/- 5.703 ng per 150 min (n = 11). Thus, 33% of the PGF2 alpha was transported rapidly to the ovary via the systemic route, while 67% was transported by slow local countercurrent diffusion, which extended the duration of luteolytic activity to four times that of the PGF2 alpha surge. These results indicate both rapid systemic transport of PGF2 alpha to the ovaries and a slower buffer mechanism involving a local diffusion pathway, rather than a direct countercurrent system.     

Evidence for the development of tolerance to PGF2 alpha on the ethanol-induced gastric mucosal damage

PGF2 alpha, 100 micrograms/kg intraperitoneally, applied 30 min before 1.0 ml intragastric ethanol (96%) exerts cytoprotective effect on the gastric mucosal membrane. After a week long pretreatment of the animals with 0.25; 0.5 and 1.0 mg/day PGF2 alpha resulted in a diminishing cytoprotective effect. The gastric tissue cAMP level raised simultaneously and after the PGF2 alpha pretreatment with the taming cytoprotection the cAMP level diminished parallel in a dose dependent manner. It is assumed that after PGF2 alpha pretreatment the density of the cellular PGF2 alpha receptors decreases, according to the observed phenomenon.     

Prostaglandin F2alpha-induced estrus in ewes exhibiting estrous cycles of different duration

Effects of prostaglandin F(2alpha) (PGF(2alpha)), administered during the mid-luteal phase of the estrous cycle, were examined in ewes exhibiting estrous cycles classified as short (< or =16.5 days, short-cycle ewes, n = 10) or long (> or =18 days, long-cycle ewes, n = 9) based on the durations of two estrous cycles (cycles -2 and -1) before treatment. The ewes received (i.m.) 20mg of PGF(2alpha) on day 10 of the third estrous cycle (cycle 0) followed, 36 h later, by 25 microg of gonadotropin releasing hormone (GnRH) to time the events of ovulation. Duration of subsequent estrous cycles +1 and +2 were recorded, and then the ewes were treated with the same combination of PGF(2alpha) and GnRH beginning on day 10 of estrous cycle +3. Ovaries were recovered 6h after GnRH administration to assess development of pre-ovulatory follicles. The proportion of ewes that exhibited estrus after PGF(2alpha) and GnRH treatment on cycle 0 was not different (P > 0.05) between short- and long-cycle ewes. Onset of estrus occurred sooner (P < 0.05) after PGF(2alpha) injection in short-cycle ewes than in long-cycle ewes (1.9 +/- 0.1 days and 2.3 +/- 0.1 days, duration of cycle 0 was 11.9 and 12.3 days, respectively). Duration of estrous cycle +1 was 1.2 days longer (P < 0.01) than cycle -1 in short-cycle ewes. However, duration of estrous cycle +1 did not change (P > 0.05) after PGF(2alpha) and GnRH administration in ewes having long cycles. Pre-ovulatory follicles did not differ (P > 0.05) in numbers, diameter, layers of granulosa cells nor concentrations of progesterone and estradiol-17beta in follicular fluid between short- and long-cycle ewes after PGF(2alpha) and GnRH treatment. In conclusion, ewes having short or long estrous cycles responded differently to PGF(2alpha) and GnRH treatment with respect to the interval to onset of estrus and duration of the subsequent estrous cycle.     

Secretion and metabolism of prostaglandin F2 alpha by endometrial tissue obtained at different days of the oestrous cycle in cattle

Two mature heifers were slaughtered on days 3, 6-7, 10-11, 16, 18-19 or on day 21 of the oesterus cycle. Endometrium was incubated in quadruplicates with medium-199 at 37 C and a water saturated gas phase of 95% O2 + 5% CO2. Half ml medium samples were taken after 6, 12 and 24 h of incubation for determination of PGF2 alpha and PGFM. PGF2 alpha was secreted by endometrium at each stage of the oestrous cycle. Maximal secretion was measured around oestrus (p less than 0.01) compared with days 6-16 of the cycle. Concentration of PGFM in medium had a similar trend. Highest ability of endometrium for PGF2 alpha metabolism (indicated by the ratio PGF2 alpha:PGFM) was on days 6-16 of the cycle. Data suggest that PGF2 alpha metabolism by the endometrium may depend on ovarian steroids and that this metabolism may also protect the corpus luteum from the luteolytic action of PGF2 alpha besides reduced production of this prostaglandin during the luteal phase.     

Specific PGF-2 alpha binding by the corpus luteum of the pregnant and non-pregnant mare.

The binding of prostaglandin (PG) F-2 alpha to corpora lutea (CL) from pregnant and non-pregnant Pony mares was examined. Studies of the rates of association and dissociation indicated that [3H]PGF was bound specifically and reversibly to a luteal cell membrane preparation (MP) that was isolated by high speed (100,000 g) ultracentrifugation. Various PGs and PG metabolites displaced [3H]PGF from the receptors in the following decreasing order: PGF-2 alpha greater than 13, 14-dihydro-PGF-2 alpha = 13,14-dihydro-15-keto PGF-2 alpha greater than PGD-2 greater than PGF-1 alpha = PGE-2 greater than PGE-2 beta greater than PGE-1. These data implicate the 9 alpha-OH and 5,6 cis double bond as major contributors to PGF receptor recognition. The membrane preparation appeared to contain at least two receptor populations, a high affinity, low capacity and a low affinity, high capacity receptor. The binding of PGF (pg/mg MP protein +/- s.e.m. (n)) to CL of the non-pregnant mare increased from 4.09 +/- 11.6 (4), on Day 4 after ovulation, to reach maximal levels by Day 12, 15.01 +/- 2.5 (4), and declined thereafter. In pregnancy the binding of PGF continued to increase until Day 18, reaching 27.47 +/- 1.7 (3), before it declined on Day 20. The reduction in binding by Day 16 in the non-pregnant mare may reflect the process of luteolysis, while high PGF binding capacity of CL between Days 16 and 18 of pregnancy indicated that luteal maintenance during pregnancy is not associated with a reduction of PGF binding capabilities.     

Factors influencing estrus and conception in dairy heifers after prostaglandin F2-alpha

The influence of interval between insemination (AI) and estrus on subsequent fertility of PGF(2alpha)-treated (two injections of 25 mg, 11 days apart) heifers was assessed in two experiments. In Experiment I, 240 heifers were allotted to Control (AI 8 to 16 hr after estrus detection), PGF(2alpha)-E (AI 8 to 16 hr after estrus within five days of second PGF(2alpha)) or PGF(2alpha)-T (AI 80 hr after second PGF(2alpha)). In Experiment II, 130 heifers were assigned to control (AI as before) or PGF(2alpha) (AI 72 or 80 hr after second PGF(2alpha)) with half the PGF(2alpha) heifers receiving 100 mug GnRH 72 hr after first PGF(2alpha). Heifers of both experiments that were bred at a predetermined time were arrayed by interval from AI to estrus. Conception rates of heifers detected in estrus from 32 hr before AI to 24 hr after AI did not differ (x(2)=3.35, df=5, P>0.5). The percentage of GnRH-treated heifers in estrus within five days (81.8%) was not (P>0.75) greater than those not receiving GnRH (77.3%) but they had higher (P<0.05) serum progesterone (P(4)) concentration at second PGF(2alpha) (3.17 vs 2.41 ng/ml). When P(4) values were arrayed for both groups at 1 ng intervals, the percentage of heifers exhibiting estrus increased with increasing P(4) level (P<0.05).     

Endocrine secretion of prostaglandin F2alpha in cyclic gilts is decreased by intrauterine administration of exogenous oxytocin

When administered systemically, oxytocin (OT) stimulates secretion of uterine prostaglandin F2alpha (PGF2alpha) in swine, but the role of endometrially-derived OT in control of PGF2alpha release is not clear. This study determined the effect of exogenous OT, administered into the uterine lumen of intact cyclic gilts, on PGF2alpha secretion during late diestrus. Intrauterine infusion of 40USP units OT (in 30 ml 0.9% saline) was performed for 30 min (1 ml/min) into each uterine horn between 7:00 and 9:00 h on days 10, 12, 14 and 16 after estrus. Beginning 20 min before infusion, samples of jugular venous blood were drawn at 5-10-min intervals for 140 min for quantification of 13,14-dihydro-15-keto-PGF2alpha (PGFM), the major stable metabolite of PGF2alpha. Progesterone was analyzed in samples collected 0, 60 and 120 min after initiation of OT infusion. Treatment with OT did not alter plasma concentrations of PGFM on days 10 or 12 but decreased (P<0.001) PGFM concentrations for 40 min after onset of infusion on day 16. Concentrations of PGFM also were reduced in the pre-treatment samples on day 14 (P=0.05) and day 16 (P<0.001) in OT-infused gilts. Plasma progesterone declined (P<0.01) between days 10 and 16 in control-infused gilts but did not decline until after day 14 (P<0.001) in gilts infused with OT. These results indicate that when OT is administered into the uterine lumen of pigs during late diestrus, it has an anti-luteolytic effect to reduce endocrine secretion of PGF2alpha and delay the decline in progesterone that occurs during luteolysis.     

Dose and time dependent luteotropic and luteolytic action of prostaglandin F2alpha in the luteinized rabbit ovary.

The mechanism of stimulatory and inhibitory action of PGF2alpha on ovarian steroidogenesis both under in vitro and in vivo conditions has been studied in the pseudopregnant rabbits. Short term incubation of the ovaries with PGF2alpha (2.82 times 10(-5)M) resulted in an increased synthesis of progesterone and 20alpha-OH P. The addition of PGF2alpha in the medium and further incubation of the ovaries obtained from rabbits that had been constantly infused with PGF2alpha (0.5 mug/min.) for two hours resulted in increased synthesis of these progestins. The ratio of progesterone to 20alpha -OH P was also enhanced under these conditions and thus supported the luteotropic action of small doses of PGF2 under short term incubations. However, as the amount of PGF2alpha infused was increased to 5 mug/min., the addition of PGF2alpha under in vitro conditions strikingly decreased the production of these progestins. The ratio decreased the production of these progestins. The ratio of progesterone to 20alpha -OH P was also decreased and thus was indicative of luteolytic action of higher doses of PGF2alpha. High doses of PGF2alpha (5.64 times 10(-4)M) failed to cause any significant change in the progestin synthesis under short term incubation. These results thus suggest that the luteotropic and luteolytic action of PGF2alpha in the luteinized rabbit ovary is dose and time dependent.     

Synthesis and biological properties of 16(S)-amino-PGF2 alpha methyl ester

A synthesis of 16-amino-derivatives of PGF2 alpha is reported. Introduction of an amino group into position 16 of PGF2 alpha has decreased the sensitivity of the compound to metabolic degradation. 16(S)-amino-PGF2 alpha methyl ester shows high abortifacient activity with reduced diarrhoeic side effect.     

Dependence on prolactin of the luteolytic effect of prostaglandin F2alpha in rat luteal cell cultures

Luteal regression is a multistep, prolonged process, and long-term luteal cultures are required for studying it in vitro. Cell suspensions from ovaries of superovulated rats were enriched with steroidogenic cells, seeded on laminin or fibronectin, and maintained in defined medium for up to 10 days. Progesterone secretion was much lower than that of 20alpha-dihydroprogesterone, a product of 20alpha-hydroxysteroid dehydrogenase (20alpha-HSD). Prolactin added throughout the incubation period gradually increased the percent progesterone out of total progestins to fourfold, while reducing 20alpha-HSD mRNA by 73%. Luteinizing hormone accelerated the establishment of higher percent progesterone by prolactin but by itself had no effect. Prolactin did not increase total progestin production or cytochrome P450 side-chain cleavage (P450(scc)) mRNA. Cell viability was unaffected by prolactin and/or LH. Prostaglandin F2alpha (PGF2alpha) was added 7-8 days after seeding. In prolactin-treated cells, PGF2alpha reduced steroidogenesis after 4-45 h, and at 45 h total progestins and P450(scc) mRNA were reduced by 45%. At 8-45 h PGF2alpha reduced the percent progesterone out of total progestins, and at 45 h 20alpha-HSD mRNA was doubled. In contrast, in prolactin-deprived cultures, PGF2alpha had little effect on total progestins or 20alpha-HSD mRNA but doubled P450(scc) mRNA. Phospholipase C activity was stimulated by PGF2alpha regardless of prolactin. Thus, when prolactin-treated, our cultures are a good model for mature corpora lutea challenged with PGF2alpha; the finding that without prolactin PGF2alpha has an alternative set of actions could help in identifying the signaling pathways of PGF2alpha responsible for its luteolytic effects.     

A comparison of prostaglandin F2alpha and three 16-aryloxy analogues on the isolated rabbit jejunum

Three 16-aryloxy analogues of PGF2alpha are potent, full agonists on the isolated rabbit jejunum. Their actions are more prolonged than that of PGF2alpha, and radioactive tracer studies with one of the analogues reveal a slower wash-out of the analogue compared to PGF2alpha, under superfusion conditions. During the prolonged contractile response diminished responses to PGF2alpha were obtained: this effect was investigated in terms of receptor desensitization. The actions of these analogues were also investigated on the isolated guinea-pig ileum and the rabbit oviduct in vivo.