dinoprost and sulotroban

dinoprost has been researched along with sulotroban* in 3 studies

Other Studies

3 other study(ies) available for dinoprost and sulotroban

ArticleYear
Effects of the thromboxane-receptor antagonists AH 23848 and BM 13.177 on human uteroplacental arteries.
    Obstetrics and gynecology, 1992, Volume: 80, Issue:2

    We studied the effects of the thromboxane (Tx)A2-receptor antagonists AH 23848 and BM 13.177 in small isolated human uteroplacental arteries.. Fetal stem villous arteries and maternal intramyometrial arteries were dissected from placental specimens and from myometrial biopsies obtained at cesarean or from nonpregnant women after hysterectomy. Vascular ring preparations were prepared and mounted in organ baths, and isometric tension was recorded.. AH 23848 produced competitive, concentration-dependent inhibition of responses to the TxA2-mimic U46619 in all vessel types tested. Mean (+/- standard error of the mean) pA2 values (the negative logarithm of the concentration of antagonist needed to double the half maximum response [EC50] value for U46619) were 8.69 +/- 0.16 in the stem villous arteries, 9.58 +/- 0.33 in intramyometrial arteries from term pregnant women, and 9.25 +/- 0.47 in intramyometrial arteries from nonpregnant women. In stem villous arteries, the pA2 value for BM 13.177 was 6.15 +/- 0.13, whereas these values in intramyometrial arteries could not be assessed. However, the concentrations needed to produce inhibition of U46619-induced contractions were considerably higher for BM 13.177 than for AH 23848. Both drugs inhibited responses to prostaglandin (PG)F2 alpha and PGE2 in stem villous arteries, while leaving responses to vasopressin in intramyometrial arteries unaffected. No differences in the effects of the two antagonists were found between intramyometrial arteries from nonpregnant and term pregnant women.. Our results suggest that TxA2-receptor antagonists effectively inhibit responses to TxA2 in human uteroplacental arteries, and such drugs may represent an interesting therapeutic approach in preeclampsia.

    Topics: Adult; Arteries; Biphenyl Compounds; Dinoprost; Dinoprostone; Dose-Response Relationship, Drug; Female; Humans; In Vitro Techniques; Muscle Contraction; Placenta; Pregnancy; Prostaglandin Endoperoxides, Synthetic; Receptors, Prostaglandin; Receptors, Thromboxane; Sulfonamides; Thromboxanes; Uterus; Vasoconstriction; Vasopressins

1992
NIP-121 and cromakalim, potassium channel openers, preferentially suppress prostanoid-induced contraction of the guinea-pig isolated trachea.
    European journal of pharmacology, 1991, Dec-10, Volume: 209, Issue:1-2

    We have investigated the relaxant effect of the potassium channel openers, NIP-121 and cromakalim, on spontaneous and spasmogen-induced tone in the isolated guinea-pig trachea. NIP-121 and cromakalim fully suppressed the spontaneous tone in a concentration-dependent manner and the maximal response was 89 and 97% of that to 1 mM aminophylline. The suppressant effect of NIP-121 (pD2 7.39) was 5 times stronger than that of cromakalim (pD2 6.69). Spontaneous tone was completely inhibited by the cyclooxygenase inhibitor, indomethacin, and partially inhibited by the thromboxane A2 (TXA2) antagonist, BM13177. In the presence of indomethacin, the contraction induced by prostaglandin (PG) F2 alpha and PGD2 was reversed by BM13177 to the same extent. NIP-121 and cromakalim reversed the contraction induced by PGF2 alpha, PGD2 and the TXA2 mimetic, U46619, and the effects were more potent than those observed on the contraction induced by leukotriene (LT) D4, LTC4, histamine and acetylcholine. The maximal relaxant responses (%) induced by NIP-121 and cromakalim were 97 and 96 for PGF2 alpha, 94 and 87 for PGD2, 94 and 93 for U46619, 69 and 69 for LTD4, 75 and 58 for LTC4, 73 and 61 for histamine and 1 and 16 for acetylcholine, respectively. The relaxant effect of NIP-121 on responses to these spasmogens (pD2 7.35 for PGF2 alpha, 7.40 for PGD2, 7.31 for U46619, 7.28 for LTD4, 7.09 for LTC4, and 7.15 for histamine) was about 10-20 times stronger than the effect of cromakalim (pD2 6.23 for PGF2 alpha, 6.04 for PGD2, 6.20 for U46619, 6.01 for LTD4, 5.82 for LTC4 and 5.88 for histamine).(ABSTRACT TRUNCATED AT 250 WORDS)

    Topics: Animals; Arachidonic Acid; Benzopyrans; Cromakalim; Dinoprost; Glyburide; Guinea Pigs; Indomethacin; Male; Muscle Contraction; Muscle Relaxation; Muscle, Smooth; Oxadiazoles; Piperidines; Potassium Channels; Prostaglandin D2; Prostaglandin Endoperoxides, Synthetic; Prostaglandins; Pyrroles; Sulfonamides; Trachea

1991
Inhibitory effects of the selective thromboxane receptor antagonist BM 13.177 on platelet aggregation, vasoconstriction and sudden death.
    Biomedica biochimica acta, 1984, Volume: 43, Issue:8-9

    BM 13.177 (0.1-100 microM) produced a concentration-dependent reduction of the platelet shape change, aggregation and (3H)serotonin release induced by the stable PGH2 analogues U 46619 and U 44069 or exogenous and endogenous arachidonic acid, the latter mobilized by hydrogen peroxide or collagen. BM 13.177 (100 microM) did not inhibit the primary platelet activation by ADP, serotonin, thrombin or collagen in washed platelets or citrated PRP that had been pre-treated with ASA (acetylsalicylic acid). The formation of TXB2 triggered by 100 microM hydrogen peroxide or 10 microM arachidonic acid was not influenced by BM 13.177 (10 microM). In spiral strips of rat and rabbit aorta, BM 13.117 markedly reduced the vasoconstriction triggered by U 46619 and PGF2 alpha. BM 13.177 did not inhibit the K+-or noradrenaline-induced constriction. The concentration/response curves of the U 46619-stimulated platelet shape change and of the vasoconstriction induced by U 46619 and PGF2 alpha were shifted in parallel to the right by BM 13.177, implicating a competitive antagonism. The pAx values were about the same in these models which indicates that BM 13.177 does not differentiate between the thromboxane receptors in human platelets and rabbit aorta. In mice, BM 13.177 prevented in a dose-dependent fashion the sudden death and the symptoms of respiratory depression and shock induced by i.v. injections of U 46619 or arachidonic acid. BM 13.177 did not exert partial agonist activity in the in vitro and in the animal models.(ABSTRACT TRUNCATED AT 250 WORDS)

    Topics: 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; Animals; Aorta; Arachidonic Acid; Arachidonic Acids; Blood Platelets; Dinoprost; Humans; Platelet Aggregation; Prostaglandin Endoperoxides, Synthetic; Prostaglandins F; Rats; Receptors, Cell Surface; Receptors, Prostaglandin; Receptors, Thromboxane; Serotonin; Sulfonamides; Thromboxanes; Vasoconstriction

1984