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At least 19 recordsLinked to original sources
PubMed1971

Studies on prostaglandin antagonists.

1. Three prostaglandin antagonists have been examined for their ability to block PGE(2) and PGF(2alpha) on human, guinea-pig and isolated rat gastrointestinal muscle.2. 7-oxa-13-Prostynoic acid was either a non-selective antagonist, or was ineffective on the tissues studied; it had marked spasmogenic activity on the rat fundus.3. 1-Acetyl-2-(8-chloro-10,11-dihydrodibenz (b,f)(1,4) oxazepine-10-carbonyl) hydrazine selectively antagonized the excitatory effects of PGE(2) and PGF(2alpha) in guinea-pig and rat tissues, but not in human muscle.4. Polyphloretin phosphate selectively antagonized the excitatory effects of prostaglandins in both human and guinea-pig muscle preparations, but it caused stimulation of the rat fundus.5. All the antagonists lowered the tone in many tissues. They also reduced contractions caused by potassium.6. None of the compounds blocked the inhibitory effect of PGE(2) on intestinal circular muscle.7. The implication of these results on the nature of prostaglandin receptors, and the value of each compound as a prostaglandin antagonist are discussed.

Acetates↗
PubMed1980

The cardiac effects of prostaglandins and their modification by the prostaglandin antagonist N-0164.

The cardiac actions of a number of prostaglandins and their modification by the prostaglandin antagonist sodium p-benzyl-4-[1-oxo-2-(4-chlorobenzyl)-3-phenyl propyl]phenyl phosphonate (N-0164) was studied in the isolated guinea-pig heart. Arachidonic acid, prostaglandin (PG)E2 (0.01--1 micrograms) and prostacyclin (0.01--10 micrograms), administered by bolus injection, caused dose-dependent increases in coronary flow rate, whereas PGD2, PGF2 alpha and the stable PG enderoperoxide analog U46619 (0.01--100 micrograms) caused dose-dependent decreases in coronary flow rate. Over the dose range studied, PGE2, arachidonic acid, prostacyclin and PGF2 alpha increased the sinus rate and PGD2 decreased the sinus rate, whereas U46619 had no consistent effect. Arachidonic acid, PGF2 alpha, PGD2 and U46619 produced a decrease in ventricular contractile force, whereas PGE2 had no effect and prostacyclin produced a modest increase in ventricular contractile force. N-0164 (10 ng and 100 ng/ml) selectively antagonized the coronary vasoconstrictor effects of PGD2 and PGF2 alpha. N-0164, at higher concentrations (1 micrograms/ml), antagonized the coronary vasodilator actions of PGE2; however, it did not modify the coronary vasodilator action of prostacyclin. N-0164 (10--100 ng/ml) also antagonized as a function of its concentration sinus rate changes produced by either PGD2 or PGF2 alpha, whereas at higher concentrations (1 microgram/ml), rather than antagonizing it potentiated sinus rate increases produced by either PGE2 or prostacyclin. These results suggest that the cardiac actions of prostaglandins are complex and are not readily elucidated by the use of the prostaglandin antagonist, N-0164.

Animals↗
PubMed1987

The antinociceptive effects of prostaglandin antagonists in the rat.

This study examined the antinociceptive effects of two prostaglandin antagonists, SC-25469 and SC-19220 in the rat. SC-25469 and SC-19220 inhibited acetic acid-induced writhing with ED50 s of 6.9 and 6.8 mg/kg p.o., respectively. When compared to other analgesics, the rank order of potency in the writhing test was morphine greater than pentazocine = U-50,488 greater than SC-25469 = SC-19220 greater than ibuprofen greater than aspirin greater than acetaminophen. SC-25469 (150 and 300 mg/kg p.o.) and SC-19220 (50-300 mg/kg p.o.) also suppressed the behavioral response to s.c. injection of formalin, as did aspirin (50-150 mg/kg p.o.), ibuprofen (25-100 mg/kg p.o.) and acetaminophen (300 mg/kg p.o.). However, the suppression was not of the magnitude observed after administration of morphine (ED50: 0.9 mg/kg s.c.), pentazocine (ED50: 2.4 mg/kg s.c.) or U-50,488 (ED50: 0.8 mg/kg s.c.). This study demonstrates the antinociceptive properties of prostaglandin antagonists in two distinct tests of nociception.

Acetaminophen↗
PubMed1975

Effects of prostaglandin antagonist SC-19220 on body temperature and on hyperthermic responses to prostaglandin E-1 and leukocytic pyrogen in the cat.

Intravenous injection of SC-19220 (3-9 mg/kg) caused dose-related hypothermic responses in cats. Repeated administration of SC-19220 resulted in tolerance to its hypothermic action. During SC-19220-induced hypothermia, the hyperthermic activity of both prostaglandin E-1 and leukocytic pyrogen was reduced or abolished. Neither prostaglandin E-1 nor leukocytic pyrogen was antagonized when given shortly after recovery from SC-19220-induced hypothermia or by doses of SC-19220 which did not cause hypothermia. Although these results may indicate a role of prostaglandins in normal physiological thermoregulation, it is also possible that production of hypothermia by SC-19220 is unrelated to prostaglandin antagonism.

Animals↗
PubMed1991

Organic vs functional obstruction of the fallopian tubes: differentiation with prostaglandin antagonist- and beta 2-agonist-mediated hysterosalpingography and selective ostial salpingography.

In order to determine the prevalence and cause of functional vs organic obstruction of the fallopian tubes, hysterosalpingography was repeated after pharmacologic manipulation with a prostaglandin antagonist (aspirin) and/or a beta 2-agonist (terbutaline) in 100 patients in whom the fallopian tubes did not fill with contrast medium on the initial hysterosalpingogram. Selective ostial salpingography was performed in those in whom the fallopian tubes did not fill on the second hysterosalpingogram. Patients referred from three infertility clinics were included in the study if they could be rescheduled for a second hysterosalpingogram after at least 1 week of preparation with aspirin. Hysterosalpingograms obtained after administration of aspirin showed normal filling in 21 of 100 patients with initially obstructed tubes; the tubes filled in four more patients after administration of terbutaline. Selective ostial salpingography opacified the tubes in another 36 patients in whom the tubes had so far failed to fill. On the basis of the radiographic appearance and sometimes laparoscopic observation, initial nonfilling was attributed to spasma and debris in 49 patients, submucosal fibroids in six, synechiae in three, salpingitis isthmica nodosa in two, and septated uterus in one. Hysterosalpingography, after pharmacologic manipulation with aspirin and/or selective ostial salpingography, revealed false-positive and functional tube obstructions in 61 of 100 patients. Moreover, the radiologic appearance improved categorization of organic obstructions.

Adrenergic beta-Agonists↗
PubMed1977

Adenosine as a natural prostaglandin antagonist in vascular smooth muscle.

Adenosine has actions on smooth muscle similar to those of prostaglandin (PG) antagonists. Like some PG antagonists it is a phosphodiesterase inhibitor and seems to interfere with calcium effects. It has agonist/antagonist interactions with theophylline, a PG antagonist. In rat mesenteric vascular smooth muscle adenosine blocked responses to noradrenaline which depend on release of intracellular calcium but not those to potassium ions which depend on calcium entry from extracellular fluid. Partial inhibition of endogenous PG synthesis by indomethacin enhanced the adenosine effect. In preparations in which vascular reactivity had been abolished by indomethacin and then partly restored by 1 or 5 ng/ml PG2, adenosine also inhibited responses to noradrenaline: the curve for the 5 ng/ml PG2 concentration was to the right of and parallel to the 1 ng/ml curve consistent with a competitive interaction between adenosine and PG2. Similar interactions between adenosine and PG2 were shown in human lymphocytes in which activation also depends on calcium release. These findings suggest how calcium-dependent metabolic responses may be controlled and indicate further reasons for caution in the interpretation of cyclic AMP experiments.

Adenosine↗
PubMed1995

Effects of prostaglandin antagonist phloretin derivatives on mouse ear edema induced with different skin irritants.

Edema was induced in one ear of male mice of the CFLP strain with solutions of different skin irritants (croton oil 10 microL/35 micrograms, dithranol 10 microL/30 micrograms, capsaicin 10 microL/40 micrograms or arachidonic acid to 10 microL/2 mg per ear). Edema, determined by the edema-disk gravimetric technique, was inhibited in a dose-dependent manner by the intraperitoneally administered prostaglandin antagonists polyphloretin phosphate (PPP) or di-4-phloretin phosphate (DPP). With croton oil-induced mouse ear edema, DPP 10 mg/kg caused a 38% inhibition, PPP 25 mg/kg a 33% inhibition. With dithranol-induced edema DPP 0.5 mg/kg caused a 57% inhibition, while PPP 25 mg/kg was needed to exert a similar effect. Doses of DPP and PPP needed to cause a > 40% inhibition of edema were 10 mg/kg and 25 mg/kg, respectively, for capsaicin, and 25 mg/kg and 100 mg/kg for arachidonic acid. The inhibition of the ear edema by the phloretin derivatives was: dithranol > croton oil > capsaicin > arachidonic acid. This probably reflects the different contributions of prostaglandins to the inflammation.

Animals↗
PubMed1984

Desacetyl-1-nantradol: a selective prostaglandin antagonist.

Progress in understanding the action of specific prostaglandins will be facilitated by the discovery of specific antagonists to different types of prostaglandin receptors. It has been suggested that nantradol, a cannabinoid-related compound with strong analgetic properties, is an antagonist for prostaglandin receptors. The interaction of nantradol with the receptors for prostaglandin D2 and prostaglandin I2/E1 on human platelets was examined. Desacetyl-1-nantradol, the active form of the drug, blocked the binding of prostaglandin D2 to platelets and the PGD2-induced stimulation of adenylate cyclase activity, but had no effect on the interaction of prostaglandin E1 with platelets. The data support the hypothesis that desacetyl-1-nantradol binds selectively to some classes of prostaglandin receptors and also suggest that it may be useful for distinguishing among different types of prostaglandin receptors.

Adenylyl Cyclases↗
PubMed1979

The prostaglandin antagonist polyphloretin phosphate behaves as a nonspecific inhibitor of rat hepatic adenylate cyclase.

The mechanism of the nonspecific inhibitory effects of the prostaglandin antagonist polyphloretin phosphate (PPP) was studied on a partially purified adenylate cyclase preparation from rat livers, PPP in concentrations above 100 micrograms/ml reduced the enzyme activity below basal values regardless of the stimulator used. The activity of adenylate cyclase in a persistent active state due to enzyme preincubation with guanylylimidodiphosphate (Gpp(NH)p) was inhibited 5-10 times more weakly. Kinetic studies indicate that PPP does not influence directly the catalytic site for ATP. PPP seems to produce permanent enzyme inhibition which is not antagonized by repeated washing ot the enzyme preparation. The reduced catalytic activity of adenylate cyclase retains after treatment with PPP the character of its responsiveness to the stimulators, which depends on the state of the enzyme before exposure to the inhibitor.

Adenylyl Cyclase Inhibitors↗
PubMed1981

Reduction of fertility of mice by the intrauterine injection of prostaglandin antagonists.

The intrauterine injection of 7-oxa-13-prostynoic acid, 18,18,20-trimethyl PGE-2, and meclofenamic acid in mice at the expected times of implantation significantly reduced the number of implantation sites. Indomethacin was ineffective possibly because it was exposed to high pH during the preparation of the solutions for injection. It is suggested that these prostaglandin antagonists exert their antifertility action at multiple sites involving both the embryo and mother.

Animals↗