Journal articles: 'Thromboxanes – Antagonistes'

1

Hall, Steven E. "Thromboxane A2 receptor antagonists." Medicinal Research Reviews 11, no. 5 (September 1991): 503–79. http://dx.doi.org/10.1002/med.2610110504.

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Gresele, P. "Thromboxane-synthase and thromboxane A2 antagonistic drugs." Thrombosis Research 65 (January 1992): S19. http://dx.doi.org/10.1016/0049-3848(92)90352-b.

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Klar, U., J. Kuhnke, A. Pletsch, H. Rehwinkel, and R. Schreyer. "Novel prostanoid thromboxane A2 antagonists." Bioorganic & Medicinal Chemistry Letters 5, no. 12 (June 1995): 1219–24. http://dx.doi.org/10.1016/0960-894x(95)00199-4.

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TERAO, Shinji. "Thromboxane A2 synthetase inhibitors and thromboxane A2 receptor antagonists." Journal of Synthetic Organic Chemistry, Japan 45, no. 1 (1987): 2–13. http://dx.doi.org/10.5059/yukigoseikyokaishi.45.2.

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Wardle, E. N. "Phospholipid derived mediators and glomerulonephritis." Mediators of Inflammation 2, no. 2 (1993): 99–102. http://dx.doi.org/10.1155/s0962935193000134.

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The contributions made by the various eicosanoids, PAF, the HETES and the lipoxins to the pathophysiology of glomerulonephritis is reviewed. A case can be made for clinical trials of PAF, leukotriene and thromboxane antagonists. Combined thromboxane synthetase and thromboxane receptor antagonism would seem to be the more efficacious approach for the various disease entities.

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Grandoch, Maria, Christof Börgermann, Paschal Oude Weernink, Yvonne Mahlke, Benjamin Schwindenhammer, Artur-Aron Weber, Jens Fischer, Karl Jakobs, Carsten Sand, and Martina Schmidt. "8-pCPT-conjugated cyclic AMP analogs exert thromboxane receptor antagonistic properties." Thrombosis and Haemostasis 103, no. 03 (2010): 662–76. http://dx.doi.org/10.1160/th09-06-0341.

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SummaryMembrane-permeable 8-(4-chlorophenylthio)-2'-O-methyl cyclic AMP (8-pCPT-2'-O-Me-cAMP) has been shown to specifically activate cAMP-regulated Epac proteins, without direct effects on protein kinase A and protein kinase G. During isometric tension measurements in thoracic aortic rings from Wistar rats, we observed that 8-pCPT-2'-O-Me-cAMP selectively induced a rightward shift of the concentration response curve for the thromboxane mimetic U46619, without altering the contractile response to noradrenaline. We hypothesised that 8-pCPT-2'-O-Me-cAMP and similar compounds may function as direct thromboxane receptor antagonists. Indeed, in addition to 8-pCPT-2'-OMe-cAMP, also 8-pCPT-cAMP, 8-(4-chlorophenylthio)-adenosine-3',5'-cyclic monophosphorothioate, Rp-isomer (Rp-8-CPT-cAMPS) and 8-CPT-adenosine, but not 8-Bromo-2'-O-Me-cAMP, induced rightward shifts of the contractile response to U46619. Likewise, 8-pCPT-2'-O- Me-cAMP and Rp-8-CPT-cAMPS, but not 8-Bromo-2'-O-Me-cAMP, specifically reduced U46619-induced aggregation of human platelets. In addition, 8-pCPT-2'-O-Me-cAMP and Rp-8-CPT-cAMPS completely reversed U46619-induced reduction of intercellular adhesion molecule-1 expression and migration of human coronary artery endothelial cells. Most important, the cAMP analogs that reduced the contractile response to U46619 also concentration-dependently inhibited binding of the thromboxane receptor radioligand [5,6-3H]SQ29548 to human platelets. We conclude that 8-pCPT-conjugated cAMP analogs exert competitive thromboxane receptor antagonistic properties.

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HALL, S. E. "ChemInform Abstract: Thromboxane A2 Receptor Antagonists." ChemInform 22, no. 48 (August 22, 2010): no. http://dx.doi.org/10.1002/chin.199148316.

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8

Patrono, Carlo. "Thromboxane synthesis inhibitors and receptor antagonists." Thrombosis Research 57 (January 1990): 15–23. http://dx.doi.org/10.1016/0049-3848(90)90387-r.

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9

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

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Dickinson, Roger P., Kevin N. Dack, John Steele, and Michael S. Tute. "Thromboxane modulating agents. 2. Thromboxane receptor antagonists derived from the thromboxane synthase inhibitor dazmegrel." Bioorganic & Medicinal Chemistry Letters 6, no. 14 (July 1996): 1691–96. http://dx.doi.org/10.1016/0960-894x(96)00299-5.

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11

Cassin, S., G. Gause, T. Davis, M. ter Riet, and R. Baker. "Do inhibitors of lipoxygenase and cyclooxygenase block neonatal hypoxic pulmonary vasoconstriction?" Journal of Applied Physiology 66, no. 4 (April 1, 1989): 1779–84. http://dx.doi.org/10.1152/jappl.1989.66.4.1779.

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Lipoxygenase products have been suggested as mediators of the hypoxic pulmonary pressor response in newborn animals. Data supporting this suggestion are equivocal, since lipoxygenase and leukotriene receptor antagonists that have been used may produce vasodilation because of phosphodiesterase inhibition. We used a leukotriene receptor antagonist L 649923, which appears not to have smooth muscle relaxant activity. L 649923 blocks pressor responses to leukotriene D4 (LTD4) without diminishing the pressor response to hypoxia. Also, BW 755C did not block the pressor response to hypoxia in newborn sheep and goats, whereas the pressor response to LTD4 (75 ng/kg) was depressed significantly. In newborn sheep there was an augmented response to hypoxia with BW 755C, which is consistent with cyclooxygenase inhibition. Finally, the thromboxane receptor antagonist SQ 29548 was investigated in both species. With this agent the pressor response to LTD4 in contrast to that of hypoxia was completely inhibited. We conclude that thromboxanes are involved in the pressor response to LTD4 in newborn lambs and goats. These data do not support the view that leukotrienes are involved in the ovine or caprine neonatal pulmonary pressor response to hypoxia.

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12

Jones, G. L., C. G. Lane, and P. M. O'Byrne. "Effect of thromboxane antagonists on ozone-induced airway responses in dogs." Journal of Applied Physiology 69, no. 3 (September 1, 1990): 880–84. http://dx.doi.org/10.1152/jappl.1990.69.3.880.

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Airway hyperresponsiveness after inhaled ozone in dogs may occur as a result of thromboxane release in the airway. In this study, two thromboxane receptor antagonists, L-655,240 and L-670,596, were used in doses that inhibit the response to an inhaled thromboxane mimetic, U-46619, to determine further the role of thromboxane in ozone-induced airway hyperresponsiveness. Dogs were studied on 2 days separated by 1 wk. On each day, the dogs inhaled ozone (3 ppm) for 30 min. On one randomly assigned day, 10 dogs received an infusion of L-655,240 (5 mg.kg-1.h-1) and 5 dogs received an infusion of L-670,596 (1 mg.kg-1.h-1); on the other day dogs received a control infusion. Airway responses to doubling doses of acetylcholine were measured before and after inhalation of ozone and were expressed as the concentration of acetylcholine giving a rise in resistance of 5 cmH2O.l-1.s from baseline (acetylcholine provocation concentration). The development of airway hyperresponsiveness after ozone was not inhibited by the thromboxane antagonists. The mean log difference in the acetylcholine provocative concentration before and after ozone on the L-655,240 treatment day was 0.62 +/- 0.12 (SE) and on the control day was 0.71 +/- 0.12 (P = 0.48); on the L-670,596 treatment day the mean log difference was 0.68 +/- 0.15 (SE) and on the control day it was 0.75 +/- 0.19 (P = 0.45). These results do not support an important role for thromboxane in causing ozone-induced airway hyperresponsiveness.

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13

Kerr, M. B., K. Marshall, and J. Senior. "The role of thromboxane in the uterotrophic response in the gravid normotensive and spontaneously hypertensive rat." Journal of Endocrinology 135, no. 2 (November 1992): 257–61. http://dx.doi.org/10.1677/joe.0.1350257.

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ABSTRACT The role of thromboxane in the gravid normotensive (CD) and hypertensive (SHR) rat was investigated (by utilizing two thromboxane receptor-blocking drugs, EP092 and AH23848) both at mid-gestation and at term. The parameters examined were uterine blood flow (blood flows were measured by the microsphere technique) and uterine weight and placental blood flow at term, fetal mass and number. At mid-gestation EP092 significantly (P< 0·005) increased uterine blood flow in both strains whilst the increases seen with AH23848 were not statistically significant. At term (day 22 in the CD and day 23 in the SHR rat) the antagonists increased uterine blood flow in the CD rats alone. However, at this time the antagonists caused an increase in placental blood flow in both strains. Thromboxane appears to be involved in the regulation of uteroplacental blood flow. The observation that the antagonists were able to potentiate blood flow by mid-gestation may provide a clinical indication with respect to potential prophylactic use of this class of compounds in cases of pregnancy-induced hypertension in women. Journal of Endocrinology (1992) 135, 257–261

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14

Jin, Jianguo, Todd M. Quinton, Jin Zhang, Susan E. Rittenhouse, and Satya P. Kunapuli. "Adenosine diphosphate (ADP)–induced thromboxane A2generation in human platelets requires coordinated signaling through integrin αIIbβ3 and ADP receptors." Blood 99, no. 1 (January 1, 2002): 193–98. http://dx.doi.org/10.1182/blood.v99.1.193.

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Adenosine diphosphate (ADP) is a platelet agonist that causes platelet shape change and aggregation as well as generation of thromboxane A2, another platelet agonist, through its effects on P2Y1, P2Y12, and P2X1 receptors. It is now reported that both 2-propylthio-D-βγ-dichloromethylene adenosine 5′-triphosphate (AR-C67085), a P2Y12 receptor–selective antagonist, and adenosine-2′-phosphate-5′-phosphate (A2P5P), a P2Y1 receptor–selective antagonist, inhibited ADP-induced thromboxane A2 generation in a concentration-dependent manner, indicating that coactivation of the P2Y12 and P2Y1 receptors is essential for this event. SC49992, a fibrinogen receptor antagonist, blocked ADP-induced platelet aggregation and thromboxane A2 production in a concentration-dependent manner. Similarly, P2 receptor antagonists or SC49992 blocked ADP-induced arachidonic acid liberation. Whereas SC49992 blocked arachidonic acid–induced platelet aggregation, it failed to inhibit thromboxane A2 generation induced by arachidonic acid. Thus, ADP-induced arachidonic acid liberation, but not subsequent conversion to thromboxane A2, requires outside-in signaling through the fibrinogen receptor. The Fab fragment of ligand-induced binding site–6 (LIBS6) antibody, which induces a fibrinogen-binding site on the integrin αIIbβ3, caused both platelet aggregation and thromboxane A2 generation. Inhibitors of phosphoinositide 3-kinase, Syk, Src kinases, or protein tyrosine phosphatases inhibited platelet aggregation but not thromboxane A2 generation, indicating that these signaling molecules have no significant role in phospholipase A2 activation. In the presence of P2 receptor antagonists A2P5P or AR-C67085, LIBS6 failed to generate thromboxane A2, suggesting that inside-out signaling through ADP receptors is necessary for this event. It was concluded that both outside-in signaling from the fibrinogen receptor and inside-out signaling from the P2Y1 and P2Y12 receptors are necessary for phospholipase A2 activation, resulting in arachidonic acid liberation and thromboxane A2 generation.

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15

Miki, Ichiro, and Akio Ishii. "Characterization of Thromboxane A2/Prostaglandin H2 Receptors in Porcine Coronary Artery -The Inhibitory Effect of a Novel Dibenzoxepin Derivative, KW-3635." Thrombosis and Haemostasis 67, no. 05 (1992): 582–84. http://dx.doi.org/10.1055/s-0038-1648498.

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SummaryWe characterized the thromboxane A2/prostaglandin H2 receptors in porcine coronary artery. The binding of [3H]SQ 29,548, a thromboxane A2 antagonist, to coronary arterial membranes was saturable and displaceable. Scatchard analysis of equilibrium binding showed a single class of high affinity binding sites with a dissociation constant of 18.5 ±1.0 nM and the maximum binding of 80.7 ± 5.2 fmol/mg protein. [3H]SQ 29,548 binding was concentration-dependently inhibited by thromboxane A2 antagonists such as SQ 29,548, BM13505 and BM13177 or the thromboxane A2 agonists such as U46619 and U44069. KW-3635, a novel dibenzoxepin derivative, concentration-dependently inhibited the [3H]SQ 29,548 binding to thromboxane A2/prosta-glandin H2 receptors in coronary artery with an inhibition constant of 6.0 ± 0.69 nM (mean ± S.E.M.).

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Greer, I. A., J. J. Walker, M. McLaren, A. A. Calder, and C. D. Forbes. "A Comparative Study of the Effects of Adrenoceptor Antagonists on Platelet Aggregation and Thromboxane Generation." Thrombosis and Haemostasis 54, no. 02 (1985): 480–84. http://dx.doi.org/10.1055/s-0038-1657878.

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SummaryPlatelet aggregation and thromboxane A2 have been implicated in the pathogenesis of several forms of vascular disease. The aim of this study was to determine the effect of a wide range of adrenoceptor antagonists on platelet aggregation, and thromboxane A2 production, from normal human platelet rich plasma in vitro. Labetalol, pindolol and propranolol inhibited platelet aggregation to collagen in a dose dependent manner. Increasing the concentration of collagen “shifted” the dose response curve to the right. These 3 drugs also significantly inhibited thromboxane A2 generation in response to collagen but not to arachidonic acid. This effect was independent of any inhibitory effect of these drugs on platelet aggregation, and occurred at a drug concentration close to that obtained in vivo. Atenolol, metoprolol, prazosin and timolol were similarly assessed but had no effect on either platelet aggregation or thromboxane A2 generation. This ability of labetalol, pindolol, and propranolol to inhibit platelet aggregation and thromboxane generation, may be of clinical benefit in view of the increasing evidence implicating thromboxane A2 in the pathogenesis of vascular disease.

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17

KLAR, U., J. KUHNKE, A. PLETSCH, H. REHWINKEL, and R. SCHREYER. "ChemInform Abstract: Novel Prostanoid Thromboxane A2 Antagonists." ChemInform 26, no. 43 (August 17, 2010): no. http://dx.doi.org/10.1002/chin.199543267.

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18

Soifer, Scott J., Michael D. Schreiber, and Michael A. Heymann. "Leukotriene Antagonists Attenuate Thromboxane-Inducible Pulmonary Hypertension." Pediatric Research 26, no. 2 (August 1989): 83–87. http://dx.doi.org/10.1203/00006450-198908000-00001.

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19

Cimetière, Bernard, Thierry Dubuffet, Caroline Landras, Jean-Jacques Descombes, Serge Simonet, Tony J. Verbeuren, and Gilbert Lavielle. "New tetrahydronaphthalene derivatives as combined thromboxane receptor antagonists and thromboxane synthase inhibitors." Bioorganic & Medicinal Chemistry Letters 8, no. 11 (June 1998): 1381–86. http://dx.doi.org/10.1016/s0960-894x(98)00221-2.

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20

Pace-Asciak, Cecil R., Denis Reynaud, Peter Demin, Rukshana Aslam, and Andrea Sun. "A New Family of Thromboxane Receptor Antagonists with Secondary Thromboxane Synthase Inhibition." Journal of Pharmacology and Experimental Therapeutics 301, no. 2 (May 1, 2002): 618–24. http://dx.doi.org/10.1124/jpet.301.2.618.

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21

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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22

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 (March 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 doses studied, decreased or abolished responses to angiotensin II. Losartan, but not candesartan, and only in a higher dose, produced small, but statistically significant, reductions in pressor responses to U46619 and to norepinephrine in the pulmonary and systemic vascular beds. Furthermore, losartan significantly reduced arachidonic acid-induced platelet aggregation, whereas candesartan had no effect. Pressor responses to angiotensin II were not changed by thromboxane and alpha-adrenergic receptor antagonists, or by cyclooxygenase and NO synthase inhibitors. These results show that losartan and candesartan are potent selective AT1 receptor antagonists in the pulmonary and systemic vascular beds and that losartan can attenuate thromboxane and alpha-adrenergic responses when administered at a high dose, whereas candesartan in the highest dose studied had no effect on responses to U46619 or to norepinephrine. The present data show that the effects of losartan and candesartan on vasoconstrictor responses are different and that pulmonary and systemic pressor responses to angiotensin II are not modulated or mediated by the release of cyclooxygenase products, activation of TP receptors, or the release of NO in the anesthetized rat.

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23

Mest, H. J., A. Riedel, and E. Meyer. "PAF-antagonists and thromboxane (TX) antagonists abolish PAF-induced cardiac rhythym disturbances." Prostaglandins 35, no. 5 (May 1988): 807. http://dx.doi.org/10.1016/0090-6980(88)90177-3.

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24

Bhavaraju, Kamala, Alexander Georgakis, Jianguo Jin, Yoshiaki Tomiyama, Alan T. Nurden, Paquita Nurden, and Satya P. Kunapuli. "Antagonism of P2y12 Receptor Results in Severe Impairment of Serum Thromboxane Levels. Can We Manage Patients without Combination Therapy with Aspirin?" Blood 114, no. 22 (November 20, 2009): 4013. http://dx.doi.org/10.1182/blood.v114.22.4013.4013.

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Abstract Abstract 4013 Poster Board III-949 Anti-platelet therapy is a widely accepted treatment regimen for the management of patients with cardiovascular risks. In clinics, many patients with cardiovascular diseases are managed on a combination therapy with Aspirin and Clopidogrel. Aspirin, being a COX-1 inhibitor blocks thromboxane generation and Clopidogrel metabolite antagonizes the P2Y12 receptor (ADP receptor). Thus these drugs block the two most important platelet positive feedback mediators and prevent amplification of platelet responses. The molecular mechanism of P2Y12 receptor antagonism on impairment of serum thromboxane is not understood to-date. Understanding this mechanism will clarify the molecular effects of P2Y12 antagonists when aspirin is clinically contraindicated in patients. Hypothesis We hypothesized that P2Y12 antagonism would lead to a decrease in serum thromboxane generation. We tested our hypothesis by employing both pharmacological and molecular genetic approaches. Methods and Results Serum thromboxane levels are a cogent marker for platelet hyperreactivity. It is produced when thrombin, which is generated during coagulation cascades, acts on PAR receptors on platelets. Serum was collected from non-anticoagulated blood after clot formation, following which serum thromboxane levels were measured with ELISA. The serum thromboxane levels in mice dosed with clopidogrel (n=4) (30 mg/kg body weight) were inhibited 88.04% compared to untreated mice. In human blood treated with the active metabolites of clopidogrel (R138727) or prasugrel (R361015) (n=3) were inhibited by 83.7% and 95.1%, respectively, compared to untreated human serum (100%). We also evaluated serum thromboxane levels in P2Y receptor null mice (n=4). Where as serum thromboxane levels in P2Y1 null mice were similar to those in wild type littermates, those in the P2Y12 null mice were inhibited by 78.9%. Furthermore serum thromboxane levels in P2Y12 deficient patients previously described in France and Japan were reduced to 25.3% and 11.7%, respectively, compared to normal volunteers (100%). We had one patient who was only on clopidogrel whose serum thromboxane levels were inhibited by 92.1%, compared to normal volunteers. In a pilot study, we recruited healthy volunteers (n=6), who were given clopidogrel for a week. Serum thromboxane levels were measured before and after the administration of clopidogrel. On an average, the serum thromboxane levels in these volunteers were inhibited by 72.3% after receiving clopidogrel. Conclusions In conclusion, P2Y12 receptor antagonism alone could lead to decrease in serum thromboxane levels. Hence in future novel P2Y12 antagonists alone might offer better protection without an additional need for aspirin. Disclosures: No relevant conflicts of interest to declare.

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Steigerwald, U., U. Walter, and J. Kössler. "Anticoagulants of primary haemostasis." Hämostaseologie 29, no. 03 (2009): 274–78. http://dx.doi.org/10.1055/s-0037-1617031.

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SummaryInhibition of platelet function plays an important role in the treatment and secondary prevention of cardiovascular or cerebrovascular ischemic diseases. Established antiplatelet agents use different pharmacological targets for this role. Acetylic salicylic acid achieves a reduction of thromboxane A2 formation by inhibition of COX-1. Ticlopidin or clopidogrel are ADP-P2Y12 receptor antagonists. Tirofiban, abciximab or eptifibatid are used for the inhibition of the glycoprotein IIb/IIIa receptor which is activated at the surface of platelets preceding the final step of their aggregation. The mechanism of dipyridamole is based on the inhibition of adenosine uptake and of phosphodiesterase-5.Efforts are made to improve antiplatetelet therapy with the aim to find agents with favorable clinical outcome and lower bleeding risk. Current clinical studies focus on a new generation of ADP receptor antagonists (prasugrel, cangrelor and ticagrelor) as successors of ticlopidin and clopidogrel after coronary arterial interventions. Developments using platelet targets different from established drugs are thrombin receptor antagonists (like SCH530348) or thromboxane receptor antagonists (like S18886/terutroban) in patients with cerebrovascular events. Results from recent experimental studies could lead to new strategies for antiplatetelet therapy (like inhibition of GP Ib receptor, GP VI receptor, platelet-leukocyte interaction, factor XII and others) in the future.

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Misra, Raj N., Don N. Harris, Inge M. Michel, Harold J. Goldenberg, Maria L. Webb, and Baerbel R. Brown. "Interphenylene phenyl oxazoles: novel, potent thromboxane receptor antagonists." Bioorganic & Medicinal Chemistry Letters 2, no. 9 (September 1992): 937–40. http://dx.doi.org/10.1016/s0960-894x(00)80592-2.

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Auch-Schwelk, W., Z. S. Katusic, and P. M. Vanhoutte. "Thromboxane A2 receptor antagonists inhibit endothelium-dependent contractions." Hypertension 15, no. 6_pt_2 (June 1990): 699–703. http://dx.doi.org/10.1161/01.hyp.15.6.699.

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Wilkinson, A. J., C. M. Warwick, and R. H. Davies. "Electrostatic interactions and conformation of some thromboxane antagonists." International Journal of Quantum Chemistry 34, S15 (March 12, 1988): 67–84. http://dx.doi.org/10.1002/qua.560340708.

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Darius, Harald, and Allan M. Lefer. "Antiaggregatory effects of thromboxane receptor antagonists in vivo." Thrombosis Research 40, no. 5 (December 1985): 663–75. http://dx.doi.org/10.1016/0049-3848(85)90304-4.

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30

Wei, Jing, Yixi Liu, and Songqing Wang. "3D pharmacophore models for thromboxane A2 receptor antagonists." Journal of Molecular Modeling 15, no. 10 (March 5, 2009): 1185–91. http://dx.doi.org/10.1007/s00894-009-0475-4.

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31

Welch, W. J., C. S. Wilcox, and K. R. Dunbar. "Modulation of renin by thromboxane: studies with thromboxane synthase inhibitor, receptor antagonists, and mimetic." American Journal of Physiology-Renal Physiology 257, no. 4 (October 1, 1989): F554—F560. http://dx.doi.org/10.1152/ajprenal.1989.257.4.f554.

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The regulation of plasma renin activity (PRA) by thromboxane (Tx) A2 was studied in anesthetized rats by measuring PRA before and after administration of drugs that block cyclooxygenase (CO) (indomethacin [INDO], 5 mg/kg), thromboxane synthase (TS) (UK 38485 [UK], 100 mg/kg), or Tx receptors (SQ 29548 [SQ], 8 mg/kg or L 641953 [L], 50 mg/kg) or that activate Tx receptors (U 46619 [U], 10 ng.kg-1.min-1). PRA (ng ANG I.ml-1.h-1) was unaffected by vehicle; it was reduced by INDO (25 +/- 2 to 13 +/- 3, n = 13, P less than 0.001) but was increased by UK (24 +/- 3 to 50 +/- 6, n = 18, P less than 0.005), SQ (27 +/- 4 to 44 +/- 7, n = 6, P less than 0.05), and L (32 +/- 4 to 51 +/- 7, n = 10, P less than 0.05). U reduced PRA in each rat (17 +/- 3 to 10 +/- 3, n = 6, P less than 0.005). UK caused dose-dependent stimulation of PRA (mean effective dose 50 mg/kg) and inhibition of TxB2 excretion (mean inhibitory dose 15 mg/kg). After INDO, SQ no longer changed PRA (-1 +/- 10, n = 7). Prolonged administration of SQ for 4-6 days (20 mg.kg-1.day-1 ip) did not change Na+ or K+ balances, blood pressure, renal hemodynamics, or urine flow. However, SQ stimulated PRA (P less than 0.007) independent of prior salt intake. In conclusion in anesthetized rats 1) PRA is stimulated by products of CO but inhibited by products of TS and by a Tx mimetic; 2) stimulation of PRA by SQ depends on ongoing PG and Tx synthesis; 3) rise in PRA with Tx antagonists is not closely related to changes in salt balance, blood pressure, or renal hemodynamics.

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CIMETIERE, B., T. DUBUFFET, C. LANDRAS, J. J. DESCOMBES, S. SIMONET, T. J. VERBEUREN, and G. LAVIELLE. "ChemInform Abstract: New Tetrahydronaphthalene Derivatives as Combined Thromboxane Receptor Antagonists and Thromboxane Synthase Inhibitors." ChemInform 29, no. 41 (June 19, 2010): no. http://dx.doi.org/10.1002/chin.199841096.

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Shirai, M., I. Ninomiya, and K. Sada. "Thromboxane A2/endoperoxide receptors mediate cholinergic constriction of rabbit lung microvessels." Journal of Applied Physiology 72, no. 3 (March 1, 1992): 1179–85. http://dx.doi.org/10.1152/jappl.1992.72.3.1179.

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Using an X-ray television system, we directly measured the internal diameter (ID; 100–1,000 microns) of small pulmonary arteries and analyzed the effects of cyclooxygenase inhibition and thromboxane A2/prostaglandin endoperoxide (TP) receptor blockade on the ID reductions in response to vagal nerve stimulation (VNS; 16 Hz) and injection of acetylcholine (ACh; 0.3 micrograms) in anesthetized rabbits. The ID reductions of the small arteries in response to VNS and ACh were completely abolished by pretreatment with cyclooxygenase inhibitors indomethacin and meclofenamate. Those reductions were also eliminated by pretreatment with TP receptor antagonists AA-2414 and Ono 3708. Both TP receptor antagonists abolished the ID reduction to thromboxane A2 mimetic U-46619 but did not affect the reduction to norepinephrine. The ID reductions in response to VNS and ACh were eliminated by atropine. The reduction in response to VNS was abolished by hexamethonium bromide, whereas the reduction in response to ACh was not altered by hexamethonium bromide. The results indicate that vasoconstrictions of the rabbit small pulmonary arteries in response to VNS and exogenous ACh are mediated by TP receptors as well as muscarinic receptors. The data suggest that during VNS endogenous ACh acts on muscarinic receptors to constrict the small arteries mainly by generating thromboxane A2 or prostaglandin endoperoxide.

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Bhavaraju, Kamala, Soochong Kim, and Satya P. Kunapuli. "Lyn and Fyn Kinases Positively Regulate Thromboxane Generation in Platelets." Blood 110, no. 11 (November 16, 2007): 3656. http://dx.doi.org/10.1182/blood.v110.11.3656.3656.

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Abstract Src family Kinases (SFKs) are important tyrosine kinases in platelets. The family consists of 9 members (viz., Blk, Fgr, Fyn, Hck, Lck, Lyn, Src, Yes and Yrk) and many of the isoforms are expressed in platelets. SFKs are key kinases in glycoprotein (GPVI) mediated platelet activation and we have shown that these kinases play an important role in thromboxane generation. Until now, the role of specific SFKs downstream of G protein signaling in platelets is not well understood. In the present study we characterized functional roles of specific SFK members Fyn, Lyn, Lck and Src Kinases downstream of ADP receptors. Src, Lyn and Fyn are activated downstream of ADP receptors (P2Y) receptors in a time and concentration dependent manner. The presence of fibrinogen receptor antagonist, GR144053, did not affect the activation of Src and Fyn; however, Lyn is not activated in the presence of GR144053, suggesting that Lyn requires outside-in signaling for it’s activation. On the other hand, Lck kinase is not activated downstream of ADP receptors. ADP activates P2Y1 and P2Y12 receptors which in turn couple to Gq and Gi, respectively. In order to further delineate the Src activation pathways we used P2Y1 and P2Y12 receptor antagonists MRS 2179 and AR-C69931MX respectively. Src activation is not inhibited by either P2Y1 or P2Y12 receptor antagonists, suggesting that both receptors independently contribute to the activation of Src kinase. Platelets from mice deficient in Src, Fyn or Lyn were analyzed for thromboxane generation upon stimulation with ADP. Lyn and Fyn KO mice had reduced levels of thromboxane A2 compared to wild type littermates. However, thromboxane generation from platelets lacking Src was unaffected. Hence, we conclude Lyn and Fyn kinases, but not Src, positively regulate thromboxane generation downstream of ADP receptors. We also conclude that Lyn requires outside-in signaling for its activation.

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Dickinson, Roger P., Kevin N. Dack, and John Steele. "Thromboxane modulating agents. 1. Design of 1-[(arylsulfonyl)amino] alkylindole derivatives as dual thromboxane synthase inhibitor/thromboxane receptor antagonists." Bioorganic & Medicinal Chemistry Letters 5, no. 24 (December 1995): 3017–22. http://dx.doi.org/10.1016/0960-894x(95)00529-4.

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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 addition of the TRPM8 antagonist, AMTB, did not block menthol-induced membrane potential depolarizations, but TRPA1 antagonists (A967079 or HC-030031) blocked the effects of menthol, as did intracellular GDPβS. Furthermore, external and internal Ca2+ levels were found to depolarize menthol-induced membrane potentials, whereas external Na+ was not. Y-27632 (a Rho kinase inhibitor), SC-560 (a selective COX 1 inhibitor), NS-398 (a selective COX 2 inhibitor), ozagrel (a thromboxane A2 synthase inhibitor) and SQ-29548 (highly selective thromboxane receptor antagonist) were used to investigate the involvements of Rho-kinase, cyclooxygenase (COX), and the thromboxane pathway in menthol-induced membrane potential depolarizations, and all inhibitors were found to block the effect of menthol. Conclusions: These results suggest that menthol-induced membrane potential depolarizations occur in a G-protein-, Ca2+-, Rho-kinase-, COX-, and thromboxane A2-dependent manner via TRPA1 receptor in cultured ICCs in murine small intestine. The study shows ICCs are targeted by menthol and that this interaction can affect intestinal motility.

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Patrono, C. "Renal effects of thromboxane synthesis inhibitors and receptor antagonists." European Journal of Pharmacology 183, no. 1 (July 1990): 143. http://dx.doi.org/10.1016/0014-2999(90)91411-4.

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Tomiyama, Tsuyoshi, Shuichi Wakabayashi, Kazuhiro Kosakai, and Masayuki Yokota. "Azulene derivatives: new non-prostanoid thromboxane A2 receptor antagonists." Journal of Medicinal Chemistry 33, no. 9 (September 1990): 2323–26. http://dx.doi.org/10.1021/jm00171a004.

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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 (September 1, 2010): 3162–214. http://dx.doi.org/10.2174/092986710792231978.

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Narumiya, Shuh, Fumitaka Ushikubi, Masatoshi Nakajima, Masakazu Hirata, Minoru Okuma, and Motohatsu Fujiwara. "Development of thromboxane A2 antagonists and isolation of thromboxane A2 receptor in human blood platelets." Japanese Journal of Pharmacology 52 (1990): 43. http://dx.doi.org/10.1016/s0021-5198(19)54995-2.

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Pandey, Akhilesh K., Xiangling Yin, Randolph B. Schiffer, James C. Hutson, Douglas M. Stocco, Paula Grammas, and XingJia Wang. "Involvement of the Thromboxane A2 Receptor in the Regulation of Steroidogenic Acute Regulatory Gene Expression in Murine Leydig Cells." Endocrinology 150, no. 7 (March 26, 2009): 3267–73. http://dx.doi.org/10.1210/en.2008-1425.

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Recent studies suggested an involvement of thromboxane A2 in cyclooxygenase-2-dependent inhibition of steroidogenic acute regulatory (StAR) gene expression. The present study further investigated the role of thromboxane A2 receptor in StAR gene expression and steroidogenesis in testicular Leydig cells. The thromboxane A2 receptor was detected in several Leydig cell lines. Blocking thromboxane A2 binding to the receptor using specific antagonist SQ29548 or BM567 resulted in dose-dependent increases in StAR protein and steroid production in MA-10 mouse Leydig cells. The results were confirmed with Leydig cells isolated from rats. StAR promoter activity and StAR mRNA level in the cells were also increased after the treatments, suggesting an involvement of the thromboxane A2 receptor in StAR gene transcription. Furthermore study indicated that blocking the thromboxane A2 receptor reduced dosage sensitive sex reversal-adrenal hypoplasia congenita critical region on the X chromosome, gene 1 protein, a transcriptional repressor of StAR gene expression. Specific binding of the antagonists to the receptors on cellular membrane was demonstrated by binding assays using 3H-SQ29548 and binding competition between 3H-SQ29548 and BM567. Whereas SQ29548 enhanced cAMP-induced StAR gene expression, in the absence of cAMP, it was unable to increase StAR protein and steroidogenesis. However, when the receptor was blocked by the antagonist, subthreshold levels of cAMP were able to induce maximal levels of StAR protein expression, suggesting that blocking the thromboxane A2 receptor increase sensitivity of MA-10 cells to cAMP stimulation. Taken together, the results from the present and previous studies suggest an autocrine loop, involving cyclooxygenase-2, thromboxane A synthase, and thromboxane A2 and its receptor, in cyclooxygenase-2-dependent inhibition of StAR gene expression.

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Ting, Harold J., Wallace J. Murray, and Fadi T. Khasawneh. "Drug Rediscovery: Glybenclamide Exhibits Thromboxane Receptor-Dependent Antithrombotic Activity." Blood 114, no. 22 (November 20, 2009): 2994. http://dx.doi.org/10.1182/blood.v114.22.2994.2994.

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Abstract Abstract 2994 Poster Board II-971 While proper platelet function is a vital component of hemostasis, inappropriate activation of platelets contributes to occlusive disorders such as myocardial infarction, and stroke. One pathway for platelet activation involves the synthesis of the lipid mediator thromboxane A2 (TXA2), which acts by binding to its seven-transmembrane receptor (abbreviated as TPR). Although this signaling pathway participates in the genesis of thrombosis, currently, there are no TPR antagonists that are available for clinical use; and aspirin remains the sole agent targeting this pathway. However, since aspirin is associated with multiple adverse effects, there is still considerable interest in developing TPR antagonists. To this end, we took the “drug rediscovery” approach to identify TPR antagonists. Since the sulfonylurea glybenclamide appeared to possess most of the pharmacophores known to exist in the TPR antagonist SQ29,548, we predicted it would interact with TPRs (and exhibit antiplatelet/antithrombotic activity). It was found that glybenclamide: 1) inhibited human platelet aggregation induced by the TPR agonist U46619 (1μM) and the TXA2 precursor arachidonic acid (0.5mM), concentration-dependently (1-10μM); 2) displaced SQ29,548 from its binding sites; 3) lacked any detectable effects on aggregation stimulated by 15μM ADP, or the thrombin receptor activating-peptide 4 (40μM); 4) failed to raise cAMP levels; 5) selectively (at 10mg/kg) blocked mouse TPR-mediated aggregation, under ex vivo settings; 6) prolonged (at 10mg/kg) the tail bleeding time in mice; and 6) prolonged (at 10mg/kg) the time for occlusion in a mouse carotid artery thrombosis model. Taken together, these findings indicate that glybenclamide exerts inhibitory effects on platelet function by interacting with TPR, and exhibits antithrombotic activity. Thus glybenclamide, or a rationally designed derivative, has the potential to be applied in the management of thrombotic disorders. Disclosures: No relevant conflicts of interest to declare.

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Bresnahan, B. A., R. J. Roman, W. M. Bagchus, and E. A. Lianos. "Mesangial cell immune injury: effects of thromboxane receptor antagonism." Journal of the American Society of Nephrology 1, no. 8 (February 1991): 1041–47. http://dx.doi.org/10.1681/asn.v181041.

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We assessed the renal hemodynamic changes occurring acutely after glomerular mesangial cell immune injury and the effects of thromboxane receptor antagonism on these changes. A single intravenous proteinuric dose of a monoclonal antibody raised against the rat thymocyte antigen Thy 1.1 (ER4), which is also expressed in rat mesangial cells, induced acute decrements in glomerular filtration rate and in renal blood flow in male Munich-Wistar rats. One hour after administration of 4 to 6 mg/kg of ER4 antibody, glomerular filtration rate and renal blood flow decreased by 80 and 36%, respectively. These decrements were associated with significant increments in basal thromboxane B2 synthesis in isolated glomeruli and no changes in glomerular prostaglandin E2 synthesis. Pretreatment of animals with the thromboxane receptor antagonist SQ-29,548 (2 mg/kg) significantly ameliorated decrements in glomerular filtration rate and renal blood flow. Pretreatment with a structurally dissimilar thromboxane receptor antagonist, L-670,596 (3 mg/kg) had no effect. Both antagonists at the doses employed abolished the decrements in renal blood flow induced by systemic administration of the thromboxane mimetic U-46619. Whereas the SQ-29,548 antagonist had no effect on glomerular leukotriene B4 and 12-hydroxyeicosatetraenoic acid synthesis, the L-670,596 thromboxane receptor antagonist significantly inhibited glomerular synthesis of these eicosanoids in immunologically injured glomeruli. These observations indicate that in mesangial cell immune injury the protective effect of thromboxane A2 receptor antagonism on glomerular filtration rate and renal blood flow is not solely due to inhibition of the vasoconstrictor effects of thromboxane A2. An effect on the synthesis of arachidonate lipoxygenation products may also play a role.

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Campbell, I. B., E. W. Collington, H. Finch, R. Hayes, P. Lumley, K. Mills, G. M. Robertson, K. Wharton, and I. S. Watts. "Synthesis and pharmacological evaluation of combined Thromboxane receptor antagonists/thromboxane synthase inhibitors: Pyridine-containing amino-prostanoids." Bioorganic & Medicinal Chemistry Letters 1, no. 12 (January 1991): 695–98. http://dx.doi.org/10.1016/s0960-894x(01)81050-7.

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Garcia, Analia, Haripriya Shankar, Swaminathan Murugappan, Soochong Kim, and Satya P. Kunapuli. "Regulation and functional consequences of ADP receptor-mediated ERK2 activation in platelets." Biochemical Journal 404, no. 2 (May 14, 2007): 299–308. http://dx.doi.org/10.1042/bj20061584.

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We have previously shown that ADP-induced thromboxane generation in platelets requires signalling events from the Gq-coupled P2Y1 receptor (platelet ADP receptor coupled to stimulation of phospholipase C) and the Gi-coupled P2Y12 receptor (platelet ADP receptor coupled to inhibition of adenylate cyclase) in addition to outside-in signalling. While it is also known that extracellular calcium negatively regulates ADP-induced thromboxane A2 generation, the underlying mechanism remains unclear. In the present study we sought to elucidate the signalling mechanisms and regulation by extracellular calcium of ADP-induced thromboxane A2 generation in platelets. ERK (extracllular-signal-regulated kinase) 2 activation occurred when outside-in signalling was blocked, indicating that it is a downstream event from the P2Y receptors. However, blockade of either P2Y1 or the P2Y12 receptors with corresponding antagonists completely abolished ERK phosphorylation, indicating that both P2Y receptors are required for ADP-induced ERK activation. Inhibitors of Src family kinases or the ERK upstream kinase MEK [MAPK (mitogen-activated protein kinase)/ERK kinase] abrogated ADP-induced ERK phosphorylation and thromboxane A2 generation. Finally ADP- or Gi+Gz-induced ERK phosphorylation was blocked in the presence of extracellular calcium. The present studies show that ERK2 is activated downstream of P2Y receptors through a complex mechanism involving Src kinases and this plays an important role in ADP-induced thromboxane A2 generation. We also conclude that extracellular calcium blocks ADP-induced thromboxane A2 generation through the inhibition of ERK activation.

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Garcia, Analia, Haripriya Shankar, and Satya P. Kunapuli. "Mechanism of Activation and Role of Extracellular Signal Regulated Kinase in ADP-Induced Thromboxane A2 Generation in Platelets." Blood 106, no. 11 (November 16, 2005): 3567. http://dx.doi.org/10.1182/blood.v106.11.3567.3567.

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Abstract We have previously shown that ADP-induced thromboxane A2 generation in platelets requires co-ordinated signaling events from the Gq-coupled P2Y1 receptor and the Gi-coupled P2Y12 receptor in addition to outside-in signaling. It is also known that ADP-induced thromboxane A2 generation is completely abolished in the presence of extracellular calcium, but the mechanism of this negative regulation is not known. In this study we sought to identify the important signaling molecules in ADP-induced thromboxane A2 generation in platelets and characterize the regulation of these molecules by extracellular calcium. Erk2 activation occurred when outside-in signaling was blocked, indicating that it is a downstream event from the P2Y receptors. However, blockade of either P2Y1 or the P2Y12 receptors with corresponding antagonists completely abolished Erk phosphorylation, indicating that both P2Y receptors are required for ADP-induced Erk activation. However, blockade of Erk upstream kinase MEK had not effect on ADP-induced aggregation in aspirin-treated platelets, but dramatically inhibited aggregation as well as secretion in non-aspirinated platelets, suggesting that Erk might be important for thromboxane A2 generation. Finally, PP1 and PP2, inhibitors of Src family kinases, but not PP3, an inactive analog, abolished ADP-induced Erk phosphorylation and thromboxane A2 generation. Interestingly, ADP-induced Erk phosphorylation was completely inhibited in the presence of extracellular calcium, indicating that Erk is a key signaling molecule regulated by extracellular calcium in the negative regulation of thromboxane A2 generation. We conclude that Erk2 is activated downstream of P2Y receptors through a complex mechanism involving Src kinases and plays an important role in ADP-induced thromboxane A2 generation. We also conclude that extracellular calcium blocks ADP-induced thromboxane A2 generation through the inhibition of Erk activation.

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Hall, Steven E., Wen-Ching Han, Don H. Harris, Harold Goldenberg, Inge M. Michel, Hossain Monshizadegan, and Maria L. Webb. "Synthesis of pyrrolidine oxazoles as thromboxane A2/endoperoxide receptor antagonists." Bioorganic & Medicinal Chemistry Letters 3, no. 6 (June 1993): 1263–66. http://dx.doi.org/10.1016/s0960-894x(00)80328-5.

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Harrison, Peter J. "Preparation of a cyclohexanone intermediate for synthesis of thromboxane antagonists." Tetrahedron Letters 30, no. 50 (1989): 7125–28. http://dx.doi.org/10.1016/s0040-4039(01)93441-0.

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Ge, Zhi-Dong, John A. Auchampach, Galen M. Piper, and Garrett J. Gross. "Comparison of Cardioprotective Efficacy of Two Thromboxane A2 Receptor Antagonists." Journal of Cardiovascular Pharmacology 41, no. 3 (March 2003): 481–88. http://dx.doi.org/10.1097/00005344-200303000-00018.

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Misra, Raj N. "Recent progress in the clinical development of thromboxane A2receptor antagonists." Expert Opinion on Investigational Drugs 3, no. 5 (May 1994): 469–80. http://dx.doi.org/10.1517/13543784.3.5.469.

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Journal articles on the topic 'Thromboxanes – Antagonistes'

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