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1

Chen, Liying, Mina N. Salafranca, and Jawahar L. Mehta. "Cyclooxygenase inhibition decreases nitric oxide synthase activity in human platelets." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 4 (1997): H1854—H1859. http://dx.doi.org/10.1152/ajpheart.1997.273.4.h1854.

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Activity of both nitric oxide (NO) synthase (NOS) and cyclooxygenase (COX) plays an important role in the regulation of platelet function. NO has been shown to directly activate COX. This study was designed to determine whether products of the COX pathway in turn regulate NOS activity. Human platelets were incubated with aspirin, indomethacin, the selective thromboxane A2 synthase inhibitor U-63557A, or the prostaglandin H2-thromboxane A2-receptor blocker SQ-29548 for 1 h at 37°C. Multiple indexes of the activity of thel-arginine-NO pathway and changes in cytosolic Ca2+concentration ([Ca2+]i)
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2

Carter, A. J., and S. Heptinstall. "Platelet Aggregation in Whole Blood: The Role of Thromboxane A2 and Adenosine Diphosphate." Thrombosis and Haemostasis 54, no. 03 (1985): 612–16. http://dx.doi.org/10.1055/s-0038-1660081.

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SummaryThe platelet aggregation that occurred in whole blood in response to several aggregating agents (collagen, arachidonic acid, adenosine diphosphate, adrenaline and thrombin) was measured using an Ultra-Flo 100 Whole Blood Platelet Counter. The amounts of thromboxane B2 produced were measured by radioimmunoassay. The effects of various inhibitors of thromboxane synthesis and the effects of apyrase, an enzyme that destroys adenosine diphosphate, were determined.Platelet aggregation was always accompanied by the production of thromboxane B2, and the amounts produced depended on the nature a
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3

Mangino, M. J., and C. C. Chou. "Thromboxane synthesis inhibitors and postprandial jejunal capillary exchange capacity." American Journal of Physiology-Gastrointestinal and Liver Physiology 254, no. 5 (1988): G695—G701. http://dx.doi.org/10.1152/ajpgi.1988.254.5.g695.

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The effects of thromboxane synthesis inhibitors (imidazole and U 63557A; Upjohn) and the cyclooxygenase inhibitor, mefenamic acid, on jejunal capillary filtration coefficients (Kfc) were determined in dogs before and during the presence of predigested food in the jejunal lumen. The jejunal Kfc increased significantly soon after the placement of a predigested test food containing all major constituents of diet. The Kfc remained elevated as long as the food was present in the lumen (15 min). Mefenamic acid (10 mg/kg iv) did not significantly alter resting jejunal Kfc or alter the food-induced in
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4

Vermylen, Jos, and Hans Deckmyn. "Thromboxane synthase inhibitors and receptor antagonists." Cardiovascular Drugs and Therapy 6, no. 1 (1992): 29–33. http://dx.doi.org/10.1007/bf00050914.

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5

Ksander, Gary M., Mark Erion, Andrew M. Yuan, et al. "Dual Angiotensin Converting Enzyme/Thromboxane Synthase Inhibitors." Journal of Medicinal Chemistry 37, no. 12 (1994): 1823–32. http://dx.doi.org/10.1021/jm00038a011.

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6

Shi, H., A. Yokoyama, N. Kohno, et al. "Effect of thromboxane A2 inhibitors on allergic pulmonary inflammation in mice." European Respiratory Journal 11, no. 3 (1998): 624–29. http://dx.doi.org/10.1183/09031936.98.11030624.

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Thromboxane (Tx)A2 synthase inhibitors and thromboxane prostanoid (TP) receptor antagonists have been developed as anti-asthma drugs. TxA2 may contribute to airflow limitation and bronchial hyperresponsiveness, and these compounds have been demonstrated to improve them. However, it is not known whether TxA2 is involved in bronchial inflammation. To address this question, we explored the influences of OKY-046 (a TxA2 synthase inhibitor) and S-1452 (a TP receptor antagonist) on eosinophilic inflammation of the airways using a murine model. BALB/c mice sensitized with ovalbumin and challenged by
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7

Farrukh, I. S., J. R. Michael, W. R. Summer, N. F. Adkinson, and G. H. Gurtner. "Thromboxane-induced pulmonary vasoconstriction: involvement of calcium." Journal of Applied Physiology 58, no. 1 (1985): 34–44. http://dx.doi.org/10.1152/jappl.1985.58.1.34.

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Infusion of tert-butyl hydroperoxide (t-bu-OOH) or arachidonic acid into rabbit pulmonary arteries stimulated thromboxane B2 (TxB2) production and caused pulmonary vasoconstriction. Both phenomena were blocked by cyclooxygenase inhibitors or a thromboxane synthase inhibitor. The increase in pulmonary arterial pressure caused by either t-bu-OOH or arachidonic acid infusion correlated with the concentration of TxB2 in the effluent perfusate. The concentration of TxB2 in the effluent perfusate, however, was always 10-fold greater after arachidonic acid infusion. In the rabbit pulmonary vascular b
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8

Cimetière, Bernard, Thierry Dubuffet, Caroline Landras, et al. "New tetrahydronaphthalene derivatives as combined thromboxane receptor antagonists and thromboxane synthase inhibitors." Bioorganic & Medicinal Chemistry Letters 8, no. 11 (1998): 1381–86. http://dx.doi.org/10.1016/s0960-894x(98)00221-2.

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9

Gresele, Paolo, Hans Deckmyn, Giuseppe G. Nenci, and Jos Vermylen. "Thromboxane synthase inhibitors, thromboxane receptor antagonists and dual blockers in thrombotic disorders." Trends in Pharmacological Sciences 12 (January 1991): 158–63. http://dx.doi.org/10.1016/0165-6147(91)90533-x.

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10

Ackerley, Norman, Andrew G. Brewster, George R. Brown, et al. "A Novel Approach to Dual-Acting Thromboxane Receptor Antagonist/Synthase Inhibitors Based on the Link of 1,3-Dioxane-Thromboxane Receptor Antagonists and -Thromboxane Synthase Inhibitors." Journal of Medicinal Chemistry 38, no. 10 (1995): 1608–28. http://dx.doi.org/10.1021/jm00010a005.

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11

Chemtob, S., P. Hardy, D. Abran, et al. "Peroxide-cyclooxygenase interactions in postasphyxial changes in retinal and choroidal hemodynamics." Journal of Applied Physiology 78, no. 6 (1995): 2039–46. http://dx.doi.org/10.1152/jappl.1995.78.6.2039.

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To test the role of reactive oxygen species and cyclooxygenase products in the retinal hemodynamic changes induced by asphyxia, we measured retinal (RBF) and choroidal blood flows (ChBF), malondialdehyde (MDA), prostaglandin E2 (PGE2), 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha), and thromboxane B2 (TxB2) in 1- to 3-day-old pigs treated with saline, the free radical scavengers U-74389F or high-dose allopurinol, the cyclooxygenase inhibitors ibuprofen or indomethacin, or the thromboxane synthase blocker CGS-13080 before and 5 and 60 min after a 5-min period of asphyxia. In saline-treated a
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12

Faull, A. W., H. Gaskin, P. S. Hadfield, et al. "Dual-acting thromboxane receptor antagonist/synthase inhibitors: heterocyclic variations." Bioorganic & Medicinal Chemistry Letters 2, no. 10 (1992): 1181–86. http://dx.doi.org/10.1016/s0960-894x(00)80210-3.

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13

Levens, N. R., G. M. Ksander, M. B. Zimmerman, and K. M. Mullane. "Thromboxane synthase inhibition enhances action of converting enzyme inhibitors." Hypertension 13, no. 1 (1989): 51–62. http://dx.doi.org/10.1161/01.hyp.13.1.51.

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14

KSANDER, G. M., M. ERION, A. M. YUAN, et al. "ChemInform Abstract: Dual Angiotensin Converting Enzyme/Thromboxane Synthase Inhibitors." ChemInform 25, no. 44 (2010): no. http://dx.doi.org/10.1002/chin.199444174.

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15

Albuquerque, Magaly Gir�o, Carlos Rangel Rodrigues, Ricardo Bicca De Alencastro, and Eliezer J. Barreiro. "Design of new potential 5-lipoxygenase inhibitors, dual thromboxane synthase inhibitors, and thromboxane a2 receptor antagonists byAM1." International Journal of Quantum Chemistry 56, S22 (1995): 181–90. http://dx.doi.org/10.1002/qua.560560719.

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16

CIMETIERE, B., T. DUBUFFET, C. LANDRAS, et al. "ChemInform Abstract: New Tetrahydronaphthalene Derivatives as Combined Thromboxane Receptor Antagonists and Thromboxane Synthase Inhibitors." ChemInform 29, no. 41 (2010): no. http://dx.doi.org/10.1002/chin.199841096.

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17

Gao, Y., and P. M. Vanhoutte. "Responsiveness of the guinea pig trachea to stretch: role of the epithelium and cyclooxygenase products." Journal of Applied Physiology 75, no. 5 (1993): 2112–16. http://dx.doi.org/10.1152/jappl.1993.75.5.2112.

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The role of the epithelium and cyclooxygenase products was investigated in the responses of isolated airways to sudden stretch. Strips of guinea pig trachea, in some of which the epithelium had been removed mechanically, were suspended in organ chambers; isometric tension was recorded. After rapid stretching to their optimal tension, the preparations (with and without epithelium) relaxed initially and then contracted to a level close to the imposed tension. Afterward, tissues with epithelium maintained this level of tension, but those without epithelium relaxed. After treatment with papaverine
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18

Yoshizato, Kimio, Svenja Zapf, Manfred Westphal, Michael E. Berens, and Alf Giese. "Thromboxane Synthase Inhibitors Induce Apoptosis in Migration-arrested Glioma Cells." Neurosurgery 50, no. 2 (2002): 343–54. http://dx.doi.org/10.1227/00006123-200202000-00021.

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19

Hamanaka, Nobuyuki, Kanji Takahashi, Yuuki Nagao, et al. "Pharmacological evaluation of combined PGI2 agonists/thromboxane synthase inhibitors. I." Bioorganic & Medicinal Chemistry Letters 5, no. 10 (1995): 1087–90. http://dx.doi.org/10.1016/0960-894x(95)00171-o.

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20

Soyka, Rainer, Brian D. Guth, Hans M. Weisenberger, Peter Luger, and Thomas H. Müller. "Guanidine Derivatives as Combined Thromboxane A2Receptor Antagonists and Synthase Inhibitors." Journal of Medicinal Chemistry 42, no. 7 (1999): 1235–49. http://dx.doi.org/10.1021/jm9707941.

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21

Yoshizato, Kimio, Svenja Zapf, Manfred Westphal, Michael E. Berens, and Alf Giese. "Thromboxane Synthase Inhibitors Induce Apoptosis in Migration-arrested Glioma Cells." Neurosurgery 50, no. 2 (2002): 343–54. http://dx.doi.org/10.1097/00006123-200202000-00021.

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22

Kontogiorgis, C., and D. Hadjipavlou-Litina. "Thromboxane Synthase Inhibitors and Thromboxane A2 Receptor Antagonists: A Quantitative Structure Activity Relationships (QSARs) Analysis." Current Medicinal Chemistry 17, no. 28 (2010): 3162–214. http://dx.doi.org/10.2174/092986710792231978.

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23

Weber, C., J. R. Beetens, R. Van De Wiele, M. H??ller, and F. De Clerck. "Production of thromboxane and prostaglandins in human blood in the presence of thromboxane synthase inhibitors." Blood Coagulation & Fibrinolysis 2, no. 1 (1991): 7–16. http://dx.doi.org/10.1097/00001721-199102000-00002.

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24

Rola-Pleszczynski, M., L. Gagnon, D. Bolduc, and G. LeBreton. "Evidence for the involvement of the thromboxane synthase pathway in human natural cytotoxic cell activity." Journal of Immunology 135, no. 6 (1985): 4114–19. http://dx.doi.org/10.4049/jimmunol.135.6.4114.

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Abstract We and other investigators have recently shown that inhibitors of lipoxygenase reversibly inhibit natural cytotoxic (NC) or natural killer (NK) cell activity, whereas some inhibitors of cyclooxygenase enhance these functions. In addition, exogenous LTB4 augments NC and NK activity, whereas PGE2 depresses it. In the present studies, we sought to investigate the possible role of the TxA2 synthase pathway in NC function. Inhibition of this pathway by OKY-1581 or dazoxiben significantly inhibited NC activity against HSV-infected cells as well as NK function against K562 target cells. The
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25

Ali, A., A. W. Ford-Hutchinson, and D. W. Nicholson. "Activation of protein kinase C down-regulates leukotriene C4 synthase activity and attenuates cysteinyl leukotriene production in an eosinophilic substrain of HL-60 cells." Journal of Immunology 153, no. 2 (1994): 776–88. http://dx.doi.org/10.4049/jimmunol.153.2.776.

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Abstract An eosinophilic substrain of HL-60 cells (HL-60#7) predominantly synthesized cysteinyl leukotrienes after stimulation with the calcium ionophore A23187. Activation of protein kinase C (PKC) by phorbol 12-myristate 13-acetate (PMA) specifically attenuated cysteinyl leukotriene production without affecting the biosynthesis of non-cysteinyl leukotrienes. The inhibition of cysteinyl leukotriene biosynthesis was prevented only by specific PKC inhibitors (staurosporine and bisindolylmaleimide) but not by inhibitors of tyrosine kinases (genistein, tyrphostin 47, and herbimycin A), protein ki
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26

Campbell, I. B., E. W. Collington, H. Finch, et al. "Synthesis and pharmacological evaluation of combined Thromboxane receptor antagonists/thromboxane synthase inhibitors: Pyridine-containing amino-prostanoids." Bioorganic & Medicinal Chemistry Letters 1, no. 12 (1991): 695–98. http://dx.doi.org/10.1016/s0960-894x(01)81050-7.

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27

Johnson, Roy A., Eldon G. Nidy, James W. Aiken, Norman J. Crittenden, and Robert R. Gorman. "Thromboxane A2 synthase inhibitors. 5-(3-Pyridylmethyl)benzofuran-2-carboxylic acids." Journal of Medicinal Chemistry 29, no. 8 (1986): 1461–68. http://dx.doi.org/10.1021/jm00158a024.

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28

Ledergerber, Dorothea, Martin Frotscher, and Rolf W. Hartmann. "Novel Highly Active Thromboxane A2 Synthase Inhibitors Devoid of Carboxylic Groups." Archiv der Pharmazie 330, no. 1-2 (1997): 1–5. http://dx.doi.org/10.1002/ardp.19973300102.

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29

Kim, Hyun Jung, Jinhong Wie, Insuk So, Myeong Ho Jung, Ki-Tae Ha, and Byung Joo Kim. "Menthol Modulates Pacemaker Potentials through TRPA1 Channels in Cultured Interstitial Cells of Cajal from Murine Small Intestine." Cellular Physiology and Biochemistry 38, no. 5 (2016): 1869–82. http://dx.doi.org/10.1159/000445549.

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Background/Aims: ICCs are the pacemaker cells responsible for slow waves in gastrointestinal (GI) smooth muscle, and generate periodic pacemaker potentials in current-clamp mode. Methods: The effects of menthol on the pacemaker potentials of cultured interstitial cells of Cajal (ICCs) from mouse small intestine were studied using the whole cell patch clamp technique. Results: Menthol (1 - 10 μM) was found to induce membrane potential depolarization in a concentration-dependent manner. The effects of various TRP channel antagonists were examined to investigate the receptors involved. The additi
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30

Manley, Paul W., Nigel M. Allanson, Robert F. G. Booth, et al. "Structure-activity relationships in an imidazole-based series of thromboxane synthase inhibitors." Journal of Medicinal Chemistry 30, no. 9 (1987): 1588–95. http://dx.doi.org/10.1021/jm00392a011.

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31

Asif, Mohammad. "The Study of Pyridazine Compounds on Prostanoids: Inhibitors of COX, cAMP Phosphodiesterase, and TXA2Synthase." Journal of Chemistry 2014 (2014): 1–16. http://dx.doi.org/10.1155/2014/703238.

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The pyridazine moiety is an important structural feature of various pharmacological active compounds. Synthetic pyridazine compounds have been reported as effective antiprostaglandins (PGs), 5-lipoxygenase (5-LOX), and antiplatelet agents, that is, inhibitors of prostaglandin or cyclooxygenase (COX-I & COX-II) enzyme, platelet cAMP phosphodiesterase, and thromboxane A2 (TXA2) synthase. These compounds are selective and nonselective COX inhibitors and showed analgesic, anti-inflammatory, and antipyretic activity. Pyridazine compounds with antiplatelet agents inhibited TXA2enzyme. Pyridazine
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32

Michaux, Catherine, Jean-Michel Dogné, Stéphanie Rolin, Bernard Masereel, Johan Wouters, and François Durant. "A pharmacophore model for sulphonyl-urea (-cyanoguanidine) compounds with dual action, thromboxane receptor antagonists and thromboxane synthase inhibitors." European Journal of Medicinal Chemistry 38, no. 7-8 (2003): 703–10. http://dx.doi.org/10.1016/s0223-5234(03)00076-x.

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33

Zou, Ming-Hui, and Markus Bachschmid. "Hypoxia–Reoxygenation Triggers Coronary Vasospasm in Isolated Bovine Coronary Arteries via Tyrosine Nitration of Prostacyclin Synthase." Journal of Experimental Medicine 190, no. 1 (1999): 135–40. http://dx.doi.org/10.1084/jem.190.1.135.

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The role of peroxynitrite in hypoxia–reoxygenation-induced coronary vasospasm was investigated in isolated bovine coronary arteries. Hypoxia–reoxygenation selectively blunted prostacyclin (PGI2)-dependent vasorelaxation and elicited a sustained vasoconstriction that was blocked by a cyclooxygenase inhibitor, indomethacin, and SQ29548, a thromboxane (Tx)A2/prostaglandin H2 receptor antagonist, but not by CGS13080, a TxA2 synthase blocker. The inactivation of PGI2 synthase, as evidenced by suppressed 6-keto-PGF1α release and a decreased conversion of 14C-prostaglandin H2 into 6-keto-PGF1α, was p
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34

Muralinath, E., Devi Pooja, Chbukdhara Prasanta, et al. "Drugs Acting on Platelets." Journal of Advanced Research and Reviews in Medical & Medicine 1, no. 1 (2024): 4–7. https://doi.org/10.5281/zenodo.10715587.

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<em>Platelets are participated in blood clotting and wound healing also. Antiplatelet drugs stop the formation of blood clots. These drugs play a critical role particularly in cardio vascular diseases namely myocardial infarction and stroke. Aspirin (NSAID) is a antiplatelet drug and it stops the enzyme cyclo oxygenase (CoX), so that it blocks the synthesis of thromboxane A2, a potent platelet aggregator. Clopidogrel prasugrel are examples of ADP receptor inhibitors. These drugs interfere with ASP-mediated activation of platelets and decrease the amplification of platelet aggregation. These dr
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35

Lima, Lidia, Carlos M. Fraga, and Eliezer Barreiro. "Cysteinyl Leukotriene Receptor Antagonists and Thromboxane Synthase Inhibitors: New Targets to Treat Asthma." Current Medicinal Chemistry - Anti-Inflammatory & Anti-Allergy Agents 3, no. 1 (2004): 9–18. http://dx.doi.org/10.2174/1568014043483526.

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36

Brown, G. R., D. S. Clarke, A. W. Faull, A. J. Foubister, and M. J. Smithers. "Design of dual-acting thromboxane antagonist-synthase inhibitors by a mutual prodrug approach." Bioorganic & Medicinal Chemistry Letters 6, no. 3 (1996): 273–78. http://dx.doi.org/10.1016/0960-894x(96)00004-2.

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37

LEDERGERBER, D., M. FROTSCHER, and R. W. HARTMANN. "ChemInform Abstract: Novel Highly Active Thromboxane A2 Synthase Inhibitors Devoid of Carboxylic Groups." ChemInform 28, no. 29 (2010): no. http://dx.doi.org/10.1002/chin.199729131.

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38

Desideri, N., I. Sestili, P. Piccardoni, S. Rotondo, C. Cerletti, and M. L. Stein. "Synthesis of Some Guanylhydrazones and Imidazolinylhydrazones as Thromboxane-Synthase and Platelet Aggregation Inhibitors." Archiv der Pharmazie 325, no. 12 (1992): 773–77. http://dx.doi.org/10.1002/ardp.19923251206.

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39

Rolin, S., J. M. Dogne, C. Vastersaegher, J. Hanson, and B. Masereel. "Pharmacological evaluation of both enantiomers of (R,S)-BM-591 as thromboxane A2 receptor antagonists and thromboxane synthase inhibitors." Prostaglandins & Other Lipid Mediators 74, no. 1-4 (2004): 75–86. http://dx.doi.org/10.1016/j.prostaglandins.2004.07.007.

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40

Gordon, John B., Ted R. Halla, Candice D. Fike, and Jane A. Madden. "Mediators of alkalosis-induced relaxation in pulmonary arteries from normoxic and chronically hypoxic piglets." American Journal of Physiology-Lung Cellular and Molecular Physiology 276, no. 1 (1999): L155—L163. http://dx.doi.org/10.1152/ajplung.1999.276.1.l155.

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Alkalosis-induced relaxation was measured in precontracted arterial rings from 1-wk-old piglets exposed to normoxia or to 3 days of chronic hypoxia. In normoxic piglet arteries, alkalosis-induced relaxation was blunted in arteries without functional endothelium and in arteries treated with nitric oxide synthase or guanylate cyclase inhibitors but not in arteries treated with cyclooxygenase inhibitors or Ca2+- and ATP-dependent K+-channel inhibitors. Inhibition of voltage-dependent K+ channels with 10−3 M 4-aminopyridine also failed to block alkalosis-induced relaxation. 4-Aminopyridine at 10−2
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41

MORITA, Kunihiko, Masayuki YAMAKAWA, Tokuzo MINOUCHI, et al. "Ozagrel hydrochloride monohydrate, a thromboxane synthase inhibitor, and its metabolites as inhibitors of hepatic microsomal drug metabolism." CHEMICAL & PHARMACEUTICAL BULLETIN 37, no. 12 (1989): 3351–54. http://dx.doi.org/10.1248/cpb.37.3351.

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42

Bautista-Pérez, Rocio, Leonardo del Valle-Mondragón, Agustina Cano-Martínez, Oscar Pérez-Méndez, Bruno Escalante, and Martha Franco. "Involvement of neutral sphingomyelinase in the angiotensin II signaling pathway." American Journal of Physiology-Renal Physiology 308, no. 10 (2015): F1178—F1187. http://dx.doi.org/10.1152/ajprenal.00079.2014.

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The possibility that angiotensin II (ANG II) exerts its effects through the activation of neutral sphingomyelinase (nSMase) has not been tested in kidneys. The results of the present study provide evidence for the activity and expression of nSMase in rat kidneys. In isolated perfused rat kidney, ANG II-induced renal vasoconstriction was inhibited by GW4869, an inhibitor of nSMase. We used nSMase for investigating the signal transduction downstream of ceramide. nSMase constricted the renal vasculature. An inhibitor of ceramidase (CDase), N-oleoylethanolamine (OEA), enhanced either ANG II- or nS
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43

Gardner, I. B., D. K. Walker, M. S. Lennard, D. A. Smith, and G. T. Tucker. "Comparison of the disposition of two novel combined thromboxane synthase inhibitors/thromboxane A2receptor antagonists in the isolated perfused rat liver." Xenobiotica 25, no. 2 (1995): 185–97. http://dx.doi.org/10.3109/00498259509061844.

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44

Golino, P., G. Ambrosio, P. Gresele, et al. "The in vivo antiplatelet effects of thromboxane A2 synthase inhibitors are potentiated by simultaneous thromboxane A2/prostaglandin H2 receptor blockade." Journal of Pharmacology and Experimental Therapeutics 266, no. 2 (1993): 511–17. https://doi.org/10.1016/s0022-3565(25)38378-3.

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45

Nossaman, Bobby D., Syed R. Baber, Mohammed M. Nazim, John D. Detrolio, and Philip J. Kadowitz. "Differential effects of losartan and candesartan on vasoconstrictor responses in the ratThis paper is one of a selection of papers published in this Special Issue, entitled The Cellular and Molecular Basis of Cardiovascular Dysfunction, Dhalla 70th Birthday Tribute." Canadian Journal of Physiology and Pharmacology 85, no. 3-4 (2007): 360–71. http://dx.doi.org/10.1139/y06-087.

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Losartan has been reported to have inhibitory effects on thromboxane (TP) receptor-mediated responses. In the present study, the effects of 2 nonpeptide angiotensin II (AT1) receptor antagonists, losartan and candesartan, on responses to angiotensin II, the thromboxane A2 mimic, U46619, and norepinephrine were investigated and compared in the pulmonary and systemic vascular beds of the intact-chest rat. In this study, intravenous injections of angiotensin II, U46619, and norepinephrine produced dose-related increases in pulmonary and systemic arterial pressure. Losartan and candesartan, in the
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46

Cozzi, P., U. Branzoli, G. Carganico, et al. "N-imidazolyl derivatives of the napththalene and chroman rings as thromboxane A2 synthase inhibitors." European Journal of Medicinal Chemistry 26, no. 4 (1991): 423–33. http://dx.doi.org/10.1016/0223-5234(91)90103-t.

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47

Vezza, Roberta, Anna Mezzasoma, Gigliola Venditti, and Paolo Gresele. "Prostaglandin Endoperoxides and Thromboxane A2 Activate the same Receptor Isoforms in Human Platelets." Thrombosis and Haemostasis 87, no. 01 (2002): 114–21. http://dx.doi.org/10.1055/s-0037-1612953.

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Abstract:
SummaryArachidonic acid (AA) is a potent inducer of platelet aggregation in vitro; this activity is due to its conversion to biologically active metabolites, prostaglandin (PG) endoperoxides and thromboxane A2 (TxA2). PG endoperoxides and TxA2 are thought to act on the same receptor; however, at least two isoforms of this receptor have been identified. The aim of our work was to clarify whether endoperoxides and TxA2 activate the same or different receptor subtypes to induce aggregation and calcium movements in human platelets.AA-induced aggregation and calcium rises were still detectable in p
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48

Sathler, Plínio Cunha, Marcos Santana, André Luiz Lourenço, et al. "Human thromboxane synthase: comparative modeling and docking evaluation with the competitive inhibitors Dazoxiben and Ozagrel." Journal of Enzyme Inhibition and Medicinal Chemistry 29, no. 4 (2013): 527–31. http://dx.doi.org/10.3109/14756366.2013.817403.

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49

Martinez, Gregory R., Keith A. M. Walker, Donald R. Hirschfeld, John J. Bruno, Diana S. Yang, and Patrick J. Maloney. "3,4-Dihydroquinolin-2(1H)-ones as combined inhibitors of thromboxane A2 synthase and cAMP phosphodiesterase." Journal of Medicinal Chemistry 35, no. 4 (1992): 620–28. http://dx.doi.org/10.1021/jm00082a002.

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50

Campbell, I. B., E. W. Collington, H. Finch, et al. "Synthesis and pharmacological evaluation of combined thromboxane receptor antagonist/synthase inhibitors: pyridine-containing sulphonamido acids." Bioorganic & Medicinal Chemistry Letters 1, no. 12 (1991): 699–704. http://dx.doi.org/10.1016/s0960-894x(01)81051-9.

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