Plasma progesterone and LH concentrations in ewes after injection of an analogue of prostaglandin F-2alpha.
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Plasma progesterone and LH concentrations were monitored throughout a natural oestrous cycle in 12 Clun Forest ewes and compared to those following treatment with a single i.m. injection of 100 microng ICI 80,996, an analogoue of prostaglandin F-2alpha, given during the luteal phase of the cycle. After injection of the analogue there was a high degree of synchrony in the return of oestrus (440 +/- 1-9 h; mean +/- S.E.M.) and the timing of the LH peak (48-5 +/- 2-0 h) from injection. There were no significant differences in the plasma progesterone concentrations or in the height and duration of the preovulatory LH peak between control and treatment cycles. The technique offers the possibility of controlled ovulation in the ewe. (+info)
Periovulatory gonadotrophin and ovarian steroid patterns in sheep of breeds with differing fecundity.
(74/104)
Plasma hormone concentrations before and during luteolysis (induced by injection of a prostaglandin analogue on Day 10 or 11 of the cycle), during the period of preovulatory follicle growth and ovulation were examined in sheep with known differences in ovulation rate (Romanov, Prealpes, Romanov x Prealpes cross, Ile de France). The number of CL at the time of treatment and the ovulation rate in the ensuing cycle were established by endoscopy. Plasma concentrations of FSH, LH, progesterone and total oestrogen were measured by radioimmunoassays in the 3 days before PG injection, then hourly for the 24 h after PG injection and 2-hourly for a further period up to about 100 h after PG injection. The onset and duration of oestrus were also recorded. Although breed differences were observed for many of the features studied, only the intervals between oestrus and the LH peak and between PG injection and the LH peak were significantly correlated with ovulation rate. (+info)
Effects of prostaglandins and thromboxane analogues on bullock and dog iris sphincter preparations.
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1 The bullock iris sphincter was contracted by low concentrations of prostaglandin E2 (PGE2), 16, 16-dimethyl PGE2 and 17,18,19,20-tetranor-16-p-chlorophenoxy PGE2. Other compounds with thromboxane-like actions, for example 11,9-epoxymethano PGH2, were also potent spasmogens, ZK 36374, a stable carbacyclin, was a partial agonist on the PGE-sensitive system of this tissue. 2 The thromboxane antagonist, EP 045, had little effect on the action of PGE2 and 16,16-dimethyl PGE2 on the bullock iris. 3 The dog iris sphincter was sensitive to PGF2 alpha but not to PGE2 and 11,9-epoxymethano PGH2. 4 16,16-dimethyl PGE2 had very low activity on the dog iris in contrast to its high activity on the bullock iris. The reverse was found with the 17,18,19,20-tetranor-16-m-trifluoromethylphenoxy analogue of PGF2 alpha (ICI 81008). This indicates a considerable selectivity of action of the two analogues. 5 The results are discussed in relation to the existing knowledge of prostanoid receptors. (+info)
Thromboxane-induced phosphatidate formation in human platelets. Relationship to receptor occupancy and to changes in cytosolic free calcium.
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The inter-relationships between receptor occupancy, inositol phospholipid metabolism and elevation of cytosolic free Ca2+ in thromboxane A2-induced human platelet activation were investigated by using the stable thromboxane A2 mimetic, 9,11-epoxymethanoprostaglandin H2, and the thromboxane A2 receptor antagonist, EPO45. 9,11-Epoxymethanoprostaglandin H2 stimulated platelet phosphatidylinositol metabolism as indicated by the rapid accumulation of [32P]phosphatidate and later accumulation of [32P]phosphatidylinositol in platelets pre-labelled with [32P]Pi. These effects of 9,11-epoxymethanoprostaglandin H2 were concentration-dependent and half-maximal [32P]phosphatidate formation occurred at an agonist concentration of 54 +/- 8 nM. With platelets labelled with the fluorescent Ca2+ indicator quin 2, resting cytosolic free Ca2+ was 86 +/- 12 nM. 9,11-Epoxymethanoprostaglandin H2 induced a rapid, concentration-dependent elevation of cytosolic free Ca2+ to a maximum of 300-700 nM. Half-maximal stimulation was observed at an agonist concentration of 80 +/- 23 nM. The thromboxane A2 receptor antagonist EPO45 selectively inhibited 9,11-epoxymethanoprostaglandin H2-induced [32P]phosphatidate formation and elevation of cytosolic free Ca2+, indicating that both events are sequelae of receptor occupancy. Human platelets contain a single class of stereospecific, saturable, high affinity (KD = 70 +/- 13 nM) binding sites for 9,11-epoxymethano[3H]prostaglandin H2. The concentration-response curve for receptor occupancy (9,11-epoxymethano-[3H]prostaglandin H2 binding) is similar to that for 9,11-epoxymethanoprostaglandin H2-induced [32P]phosphatidate formation and for elevation of cytosolic free Ca2+. These observations indicate that human platelet thromboxane A2 receptor occupation is closely linked to inositol phospholipid metabolism and to elevation of cytosolic free Ca2+. Both such events may be necessary for thromboxane A2-induced human platelet activation. (+info)
Antagonism of the thromboxane-sensitive contractile systems of the rabbit aorta, dog saphenous vein and guinea-pig trachea.
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1 The thromboxane-sensitive contractile systems in spirally-cut preparations of the rabbit aorta, dog saphenous vein and guinea-pig trachea have been compared. The full or partial agonist activities of a range of bicyclic ring analogues were found to be remarkably similar on the three preparations. In addition, EP 045, a prostanoid with a phenylsemicarbazone omega-chain, blocked the action of both thromboxane A(2) (TXA(2)) and the bicyclic ring analogues. Using 11,9-epoxymethano prostaglandin H(2) as the agonist, linear Schild plots with slopes close to unity were obtained on each preparation; this suggests a competitive type of antagonism.2 Analogues of prostaglandin D(2) (PGD(2)), PGE(2) and PGF(2alpha) also contracted the three smooth muscle preparations; those analogues containing a 16-p-halophenoxy residue were highly active. On the rabbit aorta, EP 045 completely blocked the contractile actions of these agonists, perhaps indicating a single type of prostanoid receptor in this tissue. On the dog saphenous vein PGD(2), PGE(2) and 15-methyl PGE(2) exhibited relaxant activity when the tissue was partially contracted with either a thromboxane agonist or noradrenaline. On the guinea-pig trachea 16,16-dimethyl PGE(2) and the 16-p-chlorophenoxy analogue of PGE(2) were potent contractile agents whose action was not blocked by EP 045. PGE(2) and 15-methyl PGE(2) showed similar properties but exhibited relaxant activity with increasing concentrations in the organ bath. Our results indicate the presence of three types of prostanoid receptors in the guinea-pig trachea: thromboxane- and PGE-sensitive systems mediating contraction and a PGE-sensitive system mediating relaxation.3 The similarity of the thromboxane-sensitive systems in the three smooth muscle preparations is discussed with particular reference to the differences in the equilibrium dissociation constants for EP 045. (+info)
The effect of carbacyclin, a prostaglandin analogue, on adenylate cyclase activity in platelet membranes.
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The effect of carbacyclin, a chemically stable analogue of prostacyclin, on the activity of adenylate cyclase in platelet membranes was measured, and compared with the effect of PGE1. When GTP was added in concentrations up to 10 microM the activation of adenylate cyclase by carbacyclin was increased, whereas higher concentrations of GTP were inhibitory. The addition of a non-hydrolysable analogue of GDP, guanosine 5'-[beta-thio]diphosphate (GDP[beta S] ) resulted in a dose-dependent inhibition of adenylate cyclase activation by carbacyclin; this inhibition was relieved by adding increased amounts of GTP. (+info)
Suppressor effect of prostaglandins on T colony formation.
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This study evaluated the action of prostaglandins on T colony formation. A single step culture process was used which involved direct seeding of freshly isolated peripheral blood mononuclear cells (MC) in semi-solid agar culture medium containing phytohaemagglutinin (PHA). Suppression of endogenous production of prostaglandins with 10(-6) M indomethacin increased T colony formation by up to 100%. Similarly, addition of synthetic prostaglandin E (PGE) to the culture system demonstrated a dose-dependent reduction of T colony formation by PHA-stimulated non-adherent cells. The 50% inhibitory dose (ID 50) was 10(-7) M for PGE2 and 1.3 x 10(-7) M for PGE1. Prostaglandin F had no effect on T colony formation. The synthesis of PGE by adherent cells can be increased two- to three-fold in the presence of T colony promoting activity released by PHA-stimulated lymphocytes. We conclude that monocyte produced PGE is responsible for the suppressor effect exerted by these cells on T colony formation. The PGE inhibitory role is interpreted as a feedback mechanism, modulated by lymphokines released by PHA-activated lymphocytes. (+info)
Prolactin and the control of gonadotrophin secretion in the female.(80/104)