Disease relevance of prostaglandin h2

• Subsequently, peroxynitrite nitrates and inactivates PGI2 synthase, leaving unmetabolized prostaglandin H2, which causes vasospasm, platelet aggregation, and thrombus formation via the TxA2/prostaglandin H2 receptor [1].
• Increased platelet thromboxane A2/prostaglandin H2 receptors in patients with acute myocardial infarction [2].
• Cooperative mediation by serotonin S2 and thromboxane A2/prostaglandin H2 receptor activation of cyclic flow variations in dogs with severe coronary artery stenoses [3].
• Endothelin and prostaglandin H2 enhance arteriolar myogenic tone in hypertension [4].
• In the present work the influence of perfusion pressure on renal functions and renin release was studied before and after the blockade of thromboxane A2/prostaglandin H2 (TXA2/PGH2) receptors using isolated kidneys from 7-week-old genetically hypertensive (LH), normotensive (LN), and low blood pressure (LL) rats of the Lyon strain [5].

High impact information on prostaglandin h2

• Cyclooxygenases-1 and -2 (COX-1 and COX-2, also known as prostaglandin H2 synthases-1 and -2) catalyze the committed step in prostaglandin synthesis [6].
• Furthermore, the platelet and vascular actions of TXA2 can be antagonized by prostaglandin H2/TXA2-receptor antagonists [7].
• Stereospecific conversion of prostaglandin D2 to (5Z,13E)-(15S)-9 alpha-11 beta,15-trihydroxyprosta-5,13-dien-1-oic acid (9 alpha,11 beta-prostaglandin F2) and of prostaglandin H2 to prostaglandin F2 alpha by bovine lung prostaglandin F synthase [8].
• Expression of prostaglandin H2-mediated mechanism of vascular contraction in hypertensive rats. Relation to lipoxygenase and prostacyclin synthase activities [9].
• The enhanced vasoconstriction was blunted, and the group difference was eliminated by a cyclooxygenase inhibitor (0.15 +/- 0.02 versus 0.43 +/- 0.05 mN/mm, P < .05) or a thromboxane A2/prostaglandin H2 receptor blocker (0.17 +/- 0.04 versus 0.43 +/- 0.05 mN/mm, P < .05) [10].

Chemical compound and disease context of prostaglandin h2

• Cyclooxygenase-2, prostaglandin synthases, and prostaglandin H2 metabolism in traumatic brain injury in the rat [11].
• The present study was undertaken to evaluate the role of TxA2 in the development of hypertension in spontaneously hypertensive rats (SHR) by using an orally active, highly specific TxA2/prostaglandin H2 receptor antagonist S-1452 [12].
• Glomerular thromboxane A2/prostaglandin H2 receptors: characterization and effect of adriamycin-induced nephrotic syndrome [13].

Biological context of prostaglandin h2

• S-1452, a prostaglandin H2/thromboxane A2 antagonist, abolished the PAF-induced pulmonary vasoconstriction but did not block the hypotensive action of PAF [14].
• These results suggest that a single enzyme protein purified from the bovine lung catalyzes the reduction of prostaglandin D2, prostaglandin H2, and various carbonyl compounds and that prostaglandin D2 and prostaglandin H2 are metabolized at two different active sites, yielding prostaglandin F2 alpha as the reaction product [15].
• In the developing rat brain, the enzymatic formation of prostaglandin D2 from prostaglandin H2 increased 60-fold from day 12 of gestation to birth [16].
• These results suggest that occupation of prostaglandin H2/thromboxane A2 receptors, like those for other agonists, inhibits adenylate cyclase activity, which can contribute to the promotion of platelet activation [17].
• Effects of prostaglandin H2 on perinatal pulmonary circulation [18].

Anatomical context of prostaglandin h2

• Collectively, these observations suggest that arachidonic acid stimulates endothelium-dependent release from the perfused aorta of a prostanoid that contracts vascular smooth muscle via interaction with thromboxane A2/prostaglandin H2 receptors [19].
• Neither cyclooxygenase inhibition nor thromboxane A2/prostaglandin H2 antagonism blocked the decrease in coronary venous granulocyte count.(ABSTRACT TRUNCATED AT 250 WORDS)[20]
• Thromboxane A2 and prostaglandin H2 activate platelets, while endothelin has no direct platelet effects, but causes smooth muscle proliferation [21].
• Selective modulation of the human platelet thromboxane A2/prostaglandin H2 receptor by eicosapentaenoic and docosahexaenoic acids in intact platelets and solubilized platelet membranes [22].
• In contrast, addition of phorbol ester to HL-60 cells to induce differentiation into macrophages led within 4 h to a strong and preferential increase in thromboxane synthesis from prostaglandin H2, and microsomal assays disclosed a major rise in Vmax for both prostaglandin H synthase and thromboxane synthase [23].

Associations of prostaglandin h2 with other chemical compounds

• TXRBs rely for their efficacy only on blockade of the TXA2 receptor and antagonize the deleterious effects of both TXA2 and prostaglandin H2 equally, so they represent a simpler pharmacological approach than TXSIs [24].
• The inhibition of HK was specific for alpha- and gamma-thrombin-induced platelet aggregation, because HK did not inhibit platelet aggregation induced by ADP, collagen, calcium ionophore (A23187), phorbol myristate acetate (PMA), PMA + A23187, or 9,11-methano derivative of prostaglandin H2 (U46619) [25].
• The radiolabeled thromboxane A2/prostaglandin H2 (TXA2/PGH2) agonist 125I-BOP bound to the TXA2/PGH2 receptor on human platelet membranes [26].
• The two cyclooxygenase isoforms, cyclooxygenase-1 and cyclooxygenase-2, both metabolize arachidonic acid to prostaglandin H2, which is subsequently processed by downstream enzymes to the various prostanoids [27].
• These vesicles in either 80 or 2 microM flufenamate utilized NADH or NADPH as electron donor in the reductive peroxidative step of prostaglandin H2 formation [28].

Gene context of prostaglandin h2

• In addition, we tested whether the impairment is due to (i) decreased endothelial NO synthase activity, (ii) increased NO inactivation and/or (iii) increased production of the endothelium-derived constricting factors thromboxane A2/prostaglandin H2 and endothelin-1 [29].
• Several nonsteroidal anti-inflammatory drugs, stable prostaglandin H2 analogues and cysteinyl leukotrienes were screened for inhibition of PGES activity [30].
• Prostaglandin synthesis requires cyclooxygenase-1 (COX1) or -2 (COX2), which mediate the conversion of arachidonate to prostaglandin H2 [31].
• The conversion of arachidonic acid (AA) to prostaglandin H2 is catalyzed at least by two isoforms of cyclooxygenase, named Cox-1 and Cox-2 [32].
• Prostacyclin synthase (PGIS), which converts prostaglandin H2 to prostacyclin, is a member of the cytochrome P450 superfamily [33].

Analytical, diagnostic and therapeutic context of prostaglandin h2

• Thus, improvement of endothelial function was probably achieved by facilitating the action of NO at the level of the smooth muscle cells and by reducing prostaglandin H2-induced constriction [34].
• Using a polyclonal antibody against authentic thromboxane A2/prostaglandin H2 (TxA2/PGH2) receptor protein, we assessed the distribution of this receptor in the normal rat kidney by routine methods of immunofluorescence microscopy [35].
• A fast, nondestructive purification scheme for prostaglandin H2 using a nonaqueous, bonded-phase high-performance liquid chromatography system [36].
• Intravenous injection of thromboxane A2 into anaesthetized quinea pigs was followed by a pronounced increase in the tracheal insufflation pressure, potency compared to prostaglandin H2, 31-45 [37].

References