Precursors in the biosynthesis of prostaglandins and thromboxanes from arachidonic acid. They are physiologically active compounds, having effect on vascular and airway smooth muscles, platelet aggregation, etc.
A group of physiologically active prostaglandin endoperoxides. They are precursors in the biosynthesis of prostaglandins and thromboxanes. Most frequently encountered member of this group is the prostaglandin G2.
Synthetic compounds that are analogs of the naturally occurring prostaglandin endoperoxides and that mimic their pharmacologic and physiologic activities. They are usually more stable than the naturally occurring compounds.
A group of physiologically active prostaglandin endoperoxides. They are precursors in the biosynthesis of prostaglandins and thromboxanes. The most frequently encountered member of this group is the prostaglandin H2.
A group of compounds derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway. They are extremely potent mediators of a diverse group of physiological processes.
A group of compounds that contain a bivalent O-O group, i.e., the oxygen atoms are univalent. They can either be inorganic or organic in nature. Such compounds release atomic (nascent) oxygen readily. Thus they are strong oxidizing agents and fire hazards when in contact with combustible materials, especially under high-temperature conditions. The chief industrial uses of peroxides are as oxidizing agents, bleaching agents, and initiators of polymerization. (From Hawley's Condensed Chemical Dictionary, 11th ed)
A cyclic endoperoxide intermediate produced by the action of CYCLOOXYGENASE on ARACHIDONIC ACID. It is further converted by a series of specific enzymes to the series 2 prostaglandins.
An enzyme found predominantly in platelet microsomes. It catalyzes the conversion of PGG(2) and PGH(2) (prostaglandin endoperoxides) to thromboxane A2. EC 5.3.99.5.
Dibenzothiepins are a class of tricyclic heterocyclic compounds sharing a common structure of two benzene rings fused to a thiepin ring, which have been used in the development of various pharmaceutical drugs, particularly as antipsychotic agents, but are not widely used in current clinical practice due to their adverse effects profile.
(11 alpha,13E,15S)-11,15-Dihydroxy-9-oxoprost-13-en-1-oic acid (PGE(1)); (5Z,11 alpha,13E,15S)-11,15-dihydroxy-9-oxoprosta-5,13-dien-1-oic acid (PGE(2)); and (5Z,11 alpha,13E,15S,17Z)-11,15-dihydroxy-9-oxoprosta-5,13,17-trien-1-oic acid (PGE(3)). Three of the six naturally occurring prostaglandins. They are considered primary in that no one is derived from another in living organisms. Originally isolated from sheep seminal fluid and vesicles, they are found in many organs and tissues and play a major role in mediating various physiological activities.
Compounds obtained by chemical synthesis that are analogs or derivatives of naturally occurring prostaglandins and that have similar activity.
A saclike, glandular diverticulum on each ductus deferens in male vertebrates. It is united with the excretory duct and serves for temporary storage of semen. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
Arachidonic acids are polyunsaturated fatty acids, specifically a type of omega-6 fatty acid, that are essential for human nutrition and play crucial roles in various biological processes, including inflammation, immunity, and cell signaling. They serve as precursors to eicosanoids, which are hormone-like substances that mediate a wide range of physiological responses.
Hydrazines are organic compounds containing the functional group R-NH-NH2, where R represents an organic group, and are used in pharmaceuticals, agrochemicals, and rocket fuels, but can be highly toxic and carcinogenic with potential for environmental damage.
Cell surface proteins that bind THROMBOXANES with high affinity and trigger intracellular changes influencing the behavior of cells. Some thromboxane receptors act via the inositol phosphate and diacylglycerol second messenger systems.
Organic compounds containing both the hydroxyl and carboxyl radicals.
The attachment of PLATELETS to one another. This clumping together can be induced by a number of agents (e.g., THROMBIN; COLLAGEN) and is part of the mechanism leading to the formation of a THROMBUS.
A stable, physiologically active compound formed in vivo from the prostaglandin endoperoxides. It is important in the platelet-release reaction (release of ADP and serotonin).
An unstable intermediate between the prostaglandin endoperoxides and thromboxane B2. The compound has a bicyclic oxaneoxetane structure. It is a potent inducer of platelet aggregation and causes vasoconstriction. It is the principal component of rabbit aorta contracting substance (RCS).
Physiologically active compounds found in many organs of the body. They are formed in vivo from the prostaglandin endoperoxides and cause platelet aggregation, contraction of arteries, and other biological effects. Thromboxanes are important mediators of the actions of polyunsaturated fatty acids transformed by cyclooxygenase.
(9 alpha,11 alpha,13E,15S)-9,11,15-Trihydroxyprost-13-en-1-oic acid (PGF(1 alpha)); (5Z,9 alpha,11,alpha,13E,15S)-9,11,15-trihydroxyprosta-5,13-dien-1-oic acid (PGF(2 alpha)); (5Z,9 alpha,11 alpha,13E,15S,17Z)-9,11,15-trihydroxyprosta-5,13,17-trien-1-oic acid (PGF(3 alpha)). A family of prostaglandins that includes three of the six naturally occurring prostaglandins. All naturally occurring PGF have an alpha configuration at the 9-carbon position. They stimulate uterine and bronchial smooth muscle and are often used as oxytocics.
A non-steroidal anti-inflammatory agent (NSAID) that inhibits the enzyme cyclooxygenase necessary for the formation of prostaglandins and other autacoids. It also inhibits the motility of polymorphonuclear leukocytes.
Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.
Cell surface receptors that bind prostaglandins with high affinity and trigger intracellular changes which influence the behavior of cells. Prostaglandin receptor subtypes have been tentatively named according to their relative affinities for the endogenous prostaglandins. They include those which prefer prostaglandin D2 (DP receptors), prostaglandin E2 (EP1, EP2, and EP3 receptors), prostaglandin F2-alpha (FP receptors), and prostacyclin (IP receptors).
The most common and most biologically active of the mammalian prostaglandins. It exhibits most biological activities characteristic of prostaglandins and has been used extensively as an oxytocic agent. The compound also displays a protective effect on the intestinal mucosa.
The principal cyclooxygenase metabolite of arachidonic acid. It is released upon activation of mast cells and is also synthesized by alveolar macrophages. Among its many biological actions, the most important are its bronchoconstrictor, platelet-activating-factor-inhibitory, and cytotoxic effects.
(13E,15S)-15-Hydroxy-9-oxoprosta-10,13-dien-1-oic acid (PGA(1)); (5Z,13E,15S)-15-hydroxy-9-oxoprosta-5,10,13-trien-1-oic acid (PGA(2)); (5Z,13E,15S,17Z)-15-hydroxy-9-oxoprosta-5,10,13,17-tetraen-1-oic acid (PGA(3)). A group of naturally occurring secondary prostaglandins derived from PGE; PGA(1) and PGA(2) as well as their 19-hydroxy derivatives are found in many organs and tissues.
Enzyme complexes that catalyze the formation of PROSTAGLANDINS from the appropriate unsaturated FATTY ACIDS, molecular OXYGEN, and a reduced acceptor.
Cell surface receptors which bind prostaglandins with a high affinity and trigger intracellular changes which influence the behavior of cells. Prostaglandin E receptors prefer prostaglandin E2 to other endogenous prostaglandins. They are subdivided into EP1, EP2, and EP3 types based on their effects and their pharmacology.
Compounds that inhibit the action of prostaglandins.
Pentanoic acid, also known as valeric acid, is a carboxylic acid with a 5-carbon chain (C5H10O2), having a distinctive pungent and rancid odor, found in some animals' sweat, certain foods, and produced through wood fermentation.
Physiologically active prostaglandins found in many tissues and organs. They show pressor activity, are mediators of inflammation, and have potential antithrombotic effects.
A prostaglandin that is a powerful vasodilator and inhibits platelet aggregation. It is biosynthesized enzymatically from PROSTAGLANDIN ENDOPEROXIDES in human vascular tissue. The sodium salt has been also used to treat primary pulmonary hypertension (HYPERTENSION, PULMONARY).
A subtype of prostaglandin E receptors that specifically couples to GS ALPHA GTP-BINDING PROTEIN SUBUNITS and subsequently activates ADENYLYL CYCLASES. The receptor may also signal through the activation of PHOSPHATIDYLINOSITOL 3-KINASE.
An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes.
A subtype of prostaglandin E receptors that specifically couples to GS ALPHA GTP-BINDING PROTEIN SUBUNITS and subsequently activates ADENYLYL CYCLASES.
A naturally occurring prostaglandin that has oxytocic, luteolytic, and abortifacient activities. Due to its vasocontractile properties, the compound has a variety of other biological actions.
A potent vasodilator agent that increases peripheral blood flow.
A subtype of prostaglandin E receptors that specifically couples to GTP-BINDING PROTEIN ALPHA SUBUNIT, GQ and the subsequently activates TYPE C PHOSPHOLIPASES. Additional evidence has shown that the receptor can act through a calcium-dependent signaling pathway.
Analogs or derivatives of prostaglandins E that do not occur naturally in the body. They do not include the product of the chemical synthesis of hormonal PGE.
Artifactual vesicles formed from the endoplasmic reticulum when cells are disrupted. They are isolated by differential centrifugation and are composed of three structural features: rough vesicles, smooth vesicles, and ribosomes. Numerous enzyme activities are associated with the microsomal fraction. (Glick, Glossary of Biochemistry and Molecular Biology, 1990; from Rieger et al., Glossary of Genetics: Classical and Molecular, 5th ed)
A subtype of prostaglandin E receptors that specifically couples to GTP-BINDING PROTEIN ALPHA SUBUNIT, GI and subsequently inhibits ADENYLYL CYCLASES.
The prototypical analgesic used in the treatment of mild to moderate pain. It has anti-inflammatory and antipyretic properties and acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5)
An inducibly-expressed subtype of prostaglandin-endoperoxide synthase. It plays an important role in many cellular processes and INFLAMMATION. It is the target of COX2 INHIBITORS.
A group of SESQUITERPENES and their analogs that contain a peroxide group (PEROXIDES) within an oxepin ring (OXEPINS).
Chromatography on thin layers of adsorbents rather than in columns. The adsorbent can be alumina, silica gel, silicates, charcoals, or cellulose. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
Enzymes of the isomerase class that catalyze the oxidation of one part of a molecule with a corresponding reduction of another part of the same molecule. They include enzymes converting aldoses to ketoses (ALDOSE-KETOSE ISOMERASES), enzymes shifting a carbon-carbon double bond (CARBON-CARBON DOUBLE BOND ISOMERASES), and enzymes transposing S-S bonds (SULFUR-SULFUR BOND ISOMERASES). (From Enzyme Nomenclature, 1992) EC 5.3.

On the regulation of tone in vasa vasorum. (1/375)

OBJECTIVE: The vasa vasorum form a network of microvessels in and around the walls of large blood vessels and are thought to be necessary to delivery oxygenated blood to the outer parts of the vessel wall that are inadequately nourished by diffusion from luminal blood. This study was undertaken to investigate directly the mechanisms which control tone in the vasa vasorum. METHODS: Arterial vasa vasorum were dissected from the walls of porcine or bovine thoracic aorta and mounted in a tension myograph. Concentration-response curves were constructed to vasoconstrictors; endothelin-1(ET-1), noradrenaline (NA) angiotensin II (Ang II) and thromboxane A2-mimetics (U44069 or U46619) or vasodilators; substance P (SP) bradykinin (BK), calcitonin gene-related peptide (CGRP) or isoprenaline. Strips of porcine aorta were mounted in 25 ml organ baths. RESULTS: Potent concentration-dependent contraction of vasa vasorum was produced by ET-1. NA was a weak constrictor, Ang II had no effect or produced contraction that underwent tachyphylaxis and thromboxane A2-mimetics had no effect. In contrast NA, Ang II, U-44069 and ET-1 all produced potent concentration-dependent contraction of aortic strips. SP and BK produced endothelium-dependent relaxation while CGRP produced endothelium-independent relaxation of ET-1-precontracted vasa vasorum. Isoprenaline had no relaxant effect. CONCLUSIONS: We have demonstrated functional responses of arterial vasa vasorum to vasodilators and vasoconstrictors. Additionally these microvessels appear to respond to constrictors differently from the large host vessel.  (+info)

Endothelin alters the reactivity of vasa vasorum: mechanisms and implications for conduit vessel physiology and pathophysiology. (2/375)

1 The walls of certain large blood vessels are nourished by the vasa vasorum, a network of microvessels that penetrate the adventitia and media of the vessel wall. The purpose of this study was to characterize endothelin-1 (ET-1)-mediated contraction of vasa and to investigate whether threshold concentrations of ET-1 alters the sensitivity to constrictors. Arterial vasa were dissected from the walls of porcine thoracic aorta and mounted in a tension myograph. 2 ET-1 and ETB-selective agonist, sarafotoxin 6c (S6c), produced concentration-dependent contraction. ETA receptor antagonist, BQ123 (10 microM), caused a biphasic rightward shift of ET-1 response curves. ETB receptor antagonist, BQ788 (1 microM), produced a rightward shift of response curves to ET-1 and S6c of 5- and 80 fold respectively. 3 ET-1 responses were abolished in Ca2+-free PSS but unaffected by selective depletion of intracellular Ca2+ stores. Nifedipine (10 microM), an L-type Ca2+ channel blocker, attenuated ET-1 responses by 44%. Inhibition of receptor-operated Ca2+ channels or non-selective cation entry using SKF 96365 (30 microM) and Ni2+ (1 mM) respectively, attenuated ET-1 contractions by 60%. 4 ET-1 (1-3 nM) enhanced responses to noradrenaline (NA) (4 fold) but not to thromboxane A2-mimetic, whilst K+ (10-20 mM) sensitized vasa to both types of constrictor. 5 Therefore, ET-1-induced contraction of isolated vasa is mediated by ETA and ETB receptors and involves Ca2+ influx through L-type and non-L-type Ca2+ channels. Furthermore elevation of basal tone of vasa vasorum alters the profile of contractile reactivity. These results suggest that ET-1 may be an important regulator of vasa vasorum reactivity.  (+info)

Identification of the substrate interaction site in the N-terminal membrane anchor segment of thromboxane A2 synthase by determination of its substrate analog conformational changes using high resolution NMR technique. (3/375)

The present studies describe an investigation for the interaction of N-terminal membrane anchor domain of thromboxane A(2) synthase (TXAS) with its substrate analog in a membrane-bound environment using the two-dimensional NMR technique. TXAS and prostaglandin I(2) synthase (PGIS), respectively, convert the same substrate, prostaglandin H(2) (PGH(2)), to thromboxane A(2) and prostaglandin I(2), which have opposite biological functions. Our topology studies have indicated that the N-terminal region of TXAS has a longer N-terminal endoplasmic reticulum (ER) membrane anchor region compared with the same segment proposed for PGIS. The differences in their interaction with the ER membrane may have an important impact to facilitate their common substrate, PGH(2), across the membrane into their active sites from the luminal to the cytoplasmic side of the ER. To test this hypothesis, we first investigated the interaction of the TXAS N-terminal membrane anchor domain with its substrate analog. A synthetic peptide corresponding to the N-terminal membrane anchor domain (residues 1-35) of TXAS, which adopted a stable helical structure and exhibited a membrane anchor function in the membrane-bound environment, was used to interact with a stable PGH(2) analog,. High resolution two-dimensional NMR experiments, NOESY and TOCSY, were performed to solve the solution structures of in a membrane-mimicking environment using dodecylphosphocholine micelles. Different conformations were clearly observed in the presence and absence of the TXAS N-terminal membrane anchor domain. Through combination of the two-dimensional NMR experiments, completed (1)H NMR assignments of were obtained, and the data were used to construct three-dimensional structures of in H(2)O and dodecylphosphocholine micelles, showing the detailed conformation change upon the interaction with the membrane anchor domain. The observation supported the presence of a substrate interaction site in the N-terminal region. The combination of the structural information of and was able to simulate a solution structure of the unstable TXAS and PGIS substrate, PGH(2).  (+info)

Substrate binding is the rate-limiting step in thromboxane synthase catalysis. (4/375)

Thromboxane synthase (TXAS) is a "non-classical" cytochrome P450. Without any need for an external electron donor, or for a reductase or molecular oxygen, it uses prostaglandin H2 (PGH2) to catalyze either an isomerization reaction to form thromboxane A2 (TXA2) or a fragmentation reaction to form 12-l-hydroxy-5,8,10-heptadecatrienoic acid and malondialdehyde (MDA) at a ratio of 1:1:1 (TXA2:heptadecatrienoic acid:MDA). We report here kinetics of TXAS with heme ligands in binding study and with PGH2 in enzymatic study. We determined that 1) binding of U44069, an oxygen-based ligand, is a two-step process; U44069 first binds TXAS, then ligates the heme-iron with a maximal rate constant of 105-130 s(-1); 2) binding of cyanide, a carbon-based ligand, is a one-step process with k(on) of 2.4 M(-1) s(-1) and k(off) of 0.112 s(-1); and 3) both imidazole and clotrimazole (nitrogen-based ligands) bind TXAS in a two-step process; an initial binding to the heme-iron with on-rate constants of 8.4 x 10(4) M(-1) s(-1) and 1.5 x 10(5) M(-1) s(-1) for imidazole and clotrimazole, respectively, followed by a slow conformational change with off-rate constants of 8.8 s(-1) and 0.53 s(-1), respectively. The results of our binding study indicate that the TXAS active site is hydrophobic and spacious. In addition, steady-state kinetic study revealed that TXAS consumed PGH2 at a rate of 3,800 min(-1) and that the k(cat)/K(m) for PGH2 consumption was 3 x 10(6) M(-1) s(-1). Based on these data, TXAS appears to be a very efficient catalyst. Surprisingly, rapid-scan stopped-flow experiments revealed marginal absorbance changes upon mixing TXAS with PGH2, indicating minimal accumulation of any heme-derived intermediates. Freeze-quench EPR measurements for the same reaction showed minimal change of heme redox state. Further kinetic analysis using a combination of rapid-mixing chemical quench and computer simulation showed that the kinetic parameters of TXAS-catalyzed reaction are: PGH2 bound TXAS at a rate of 1.2-2.0 x 10(7) M(-1) s(-1); the rate of catalytic conversion of PGH2 to TXA2 or MDA was at least 15,000 s(-1) and the lower limit of the rates for products release was 4,000-6,000 s(-1). Given that the cellular PGH2 concentration is quite low, we concluded that under physiological conditions, the substrate-binding step is the rate-limiting step of the TXAS-catalyzed reaction, in sharp contrast with "classical" P450 enzymes.  (+info)

Regional vascular responses to thromboxane A2 analogue and their blockade with vapiprost, a selective thromboxane receptor blocking drug, in anesthetized dogs. (5/375)

Regional vascular responses to the thromboxane A2 analogue U46619 and effects of the selective thromboxane receptor blocking drug vapiprost on these responses were examined in anesthetized dogs. Hemodynamic responses to U46619 (0.5 micrograms/kg into the left atrium), norepinephrine (NE, 0.3 microgram/kg, i.v.) and angiotensin II (AII, 30 or 60 ng/kg, i.v.) were periodically tested before and after administration of vapiprost (10, 30 or 100 micrograms/kg, i.v.) or its vehicle. In the absence of vapiprost, U46619 increased total peripheral (TPR), vertebral (VR), coronary (CR) and renal (RR) vascular resistance by 60.1 +/- 4.7%, 33.6 +/- 4.9%, 15.3 +/- 1.3% and 120.8 +/- 17.4%, respectively, indicating that vasoconstrictor responses to U46619 were most prominent in the renal vascular bed as compared to those in the vertebral or coronary vasculatures. Vapiprost as well as the vehicle did not affect the base-line hemodynamics. However, vapiprost apparently inhibited the U46619-induced vasoconstriction in all measured vascular beds in a dose-related manner without attenuating vasoconstrictor responses to NE compared to the inhibitions of VR and CR. These results demonstrate that there was a regional difference both in the vasoconstrictor responses to U46619 and in the blocking effects of vapiprost, and indicate that vapiprost is a potent and selective antagonist for thromboxane receptors in vivo.  (+info)

Thromboxane receptor stimulation inhibits adenylate cyclase and reduces cyclic AMP-mediated inhibition of ADP-evoked responses in fura-2-loaded human platelets. (6/375)

Stimulation of human platelets with the thromboxane A2 analogue, U46619, after treatment with prostaglandin E1 or forskolin, reduced the inhibition of ADP-evoked Mn2+ influx and the release of Ca2+ from intracellular stores. U46619 decreased the elevated concentration of 3',5'-cyclic AMP in platelets that were pretreated with prostaglandin E1. 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.  (+info)

Structure and function of the human platelet thrombin receptor. Studies using monoclonal antibodies directed against a defined domain within the receptor N terminus. (7/375)

Based upon its recently cloned nucleotide sequence, the human platelet thrombin receptor is thought to be formed by a single polypeptide chain with seven transmembrane domains and an extracellular N terminus that can be cleaved by thrombin. As yet, however, little is known from studies of the receptor protein itself. To obtain such information, we have prepared monoclonal antibodies against a peptide corresponding to receptor residues Ser42 through Phe55, the domain immediately distal to the site of cleavage by thrombin. By flow cytometry, all of the antibodies reacted with the thrombin-responsive megakaryoblastic CHRF-288 and HEL cell lines, but not with the T-lymphoid Sup-T1 cell line. Functionally, the antibodies inhibited platelet responses to alpha-thrombin, gamma-thrombin, and trypsin, but had no effect on platelet activation by ADP, epinephrine, or the thromboxane analog U46619. Radioiodinated antibody bound to approximately 1,800 sites/platelet, a value similar to the reported number of moderate affinity thrombin binding sites per platelet. On Western blots, the antibodies recognized a 66-kDa protein in platelet, HEL, and CHRF-288 membranes. The discrepancy between this apparent size and the predicted mass of the receptor suggests that, as with other G protein-coupled receptors, one or more of the potential sites for N-linked glycosylation have been utilized. Therefore, these results suggest that: 1) the cloned thrombin receptor is involved in a broad range of platelet responses to thrombin, as well as gamma-thrombin and trypsin; 2) as predicted, the N terminus of the receptor is accessible on the platelet surface; 3) the moderate affinity thrombin binding site noted in earlier studies may be the receptor; 4) potentially as much as one third of the mass of the receptor is carbohydrate.  (+info)

Identification of a new congenital defect of platelet function characterized by severe impairment of platelet responses to adenosine diphosphate. (8/375)

This study characterizes a congenital hemorrhagic disorder caused by a platelet function defect with the following features: (1) severely impaired platelet aggregation and fibrinogen or von Willebrand factor (vWF) binding induced by adenosine diphosphate (ADP); (2) defective aggregation, release reaction, and fibrinogen or vWF binding induced by other agonists; (3) normal aggregation and release reaction induced by high concentrations of thrombin or collagen; (4) no further inhibition by ADP scavengers of aggregation, release reaction, and fibrinogen or vWF binding, comparable with those observed for normal platelets in the presence of ADP scavengers; (5) normal membrane glycoprotein (GP) composition and normal binding of the anti-GP IIb/IIIa monoclonal antibody 10E5; (6) no acceleration by ADP of binding of the anti-GP IIb/IIIa monoclonal antibody 7E3; (7) normal platelet-fibrin clot retraction if induced by thrombin or reptilase plus epinephrine, absent if induced by reptilase plus ADP; (8) no inhibition by ADP of the prostaglandin E1-induced increase in platelet cyclic adenosine monophosphate, but normal inhibition by epinephrine; (9) defective mobilization of cytoplasmic Ca2+ by ADP; (10) normal binding of 14C-ADP to fresh platelets, but defective binding of [2-3H]-ADP to formalin-fixed platelets. This congenital platelet function defect is characterized by selective impairment of platelet responses to ADP, caused by either decreased number of platelet ADP receptors or abnormalities of the signal-transduction pathway of platelet activation by ADP.  (+info)

Prostaglandin endoperoxides are short-lived, biologically active lipid compounds derived from the metabolism of arachidonic acid, an omega-6 fatty acid. They are intermediate products in the conversion of arachidonic acid to various prostaglandins and thromboxanes, which are crucial regulators of numerous physiological processes, including inflammation, blood clotting, and vascular constriction or dilation.

The two major prostaglandin endoperoxides are PGG2 (prostaglandin G2) and PGH2 (prostaglandin H2). They are synthesized from arachidonic acid by the action of an enzyme called cyclooxygenase (COX), which has two isoforms: COX-1 and COX-2. These endoperoxides can then be further metabolized into various prostaglandins and thromboxanes by specific synthases.

Prostaglandin endoperoxides are highly reactive and unstable, with a half-life of only a few seconds to minutes. Due to their instability, they cannot accumulate in tissues and must be rapidly converted into more stable downstream products for biological activity. Despite their short lifespan, prostaglandin endoperoxides play essential roles in mediating various physiological responses and are also implicated in several pathological conditions, such as pain, fever, and inflammation.

I'm sorry for any confusion, but there seems to be a mistake in your question. Prostaglandins are a group of lipid compounds that are synthesized in the body from fatty acids and have diverse hormonal-like effects in the body. They are not typically classified by a letter "G."

Prostaglandin G is an intermediate compound formed during the conversion of arachidonic acid to prostaglandins through the cyclooxygenase pathway. It is not a type or subclass of prostaglandins that has distinct medical relevance or definition. Therefore, I'm unable to provide a specific medical definition for 'Prostaglandins G.'

If you have any other questions or need clarification on a different topic, please let me know!

Prostaglandin endoperoxides are naturally occurring lipid compounds that play important roles as mediators in the body's inflammatory and physiological responses. They are intermediate products in the conversion of arachidonic acid to prostaglandins and thromboxanes, which are synthesized by the action of enzymes called cyclooxygenases (COX-1 and COX-2).

Synthetic prostaglandin endoperoxides, on the other hand, are chemically synthesized versions of these compounds. They are used in medical research and therapeutic applications to mimic or inhibit the effects of naturally occurring prostaglandin endoperoxides. These synthetic compounds can be used to study the mechanisms of prostaglandin action, develop new drugs, or as stand-in agents for the natural compounds in experimental settings.

It's important to note that while synthetic prostaglandin endoperoxides can serve as useful tools in research and medicine, they also carry potential risks and side effects, much like their naturally occurring counterparts. Therefore, their use should be carefully monitored and regulated to ensure safety and efficacy.

I'm sorry for any confusion, but "Prostaglandins H" is not a widely recognized or established medical term. Prostaglandins are a group of lipid compounds that are synthesized in the body from fatty acids and have diverse hormone-like effects in the body. They play roles in various physiological processes, including inflammation, blood flow regulation, and labor induction, among others.

Prostaglandin H is an intermediate in the conversion of arachidonic acid to prostaglandins through the cyclooxygenase pathway. However, it's not a final product or a commonly used term in medical definitions. If you have any specific questions about prostaglandins or their role in the body, I would be happy to help further clarify those topics for you!

Prostaglandins are naturally occurring, lipid-derived hormones that play various important roles in the human body. They are produced in nearly every tissue in response to injury or infection, and they have diverse effects depending on the site of release and the type of prostaglandin. Some of their functions include:

1. Regulation of inflammation: Prostaglandins contribute to the inflammatory response by increasing vasodilation, promoting fluid accumulation, and sensitizing pain receptors, which can lead to symptoms such as redness, heat, swelling, and pain.
2. Modulation of gastrointestinal functions: Prostaglandins protect the stomach lining from acid secretion and promote mucus production, maintaining the integrity of the gastric mucosa. They also regulate intestinal motility and secretion.
3. Control of renal function: Prostaglandins help regulate blood flow to the kidneys, maintain sodium balance, and control renin release, which affects blood pressure and fluid balance.
4. Regulation of smooth muscle contraction: Prostaglandins can cause both relaxation and contraction of smooth muscles in various tissues, such as the uterus, bronchioles, and vascular system.
5. Modulation of platelet aggregation: Some prostaglandins inhibit platelet aggregation, preventing blood clots from forming too quickly or becoming too large.
6. Reproductive system regulation: Prostaglandins are involved in the menstrual cycle, ovulation, and labor induction by promoting uterine contractions.
7. Neurotransmission: Prostaglandins can modulate neurotransmitter release and neuronal excitability, affecting pain perception, mood, and cognition.

Prostaglandins exert their effects through specific G protein-coupled receptors (GPCRs) found on the surface of target cells. There are several distinct types of prostaglandins (PGs), including PGD2, PGE2, PGF2α, PGI2 (prostacyclin), and thromboxane A2 (TXA2). Each type has unique functions and acts through specific receptors. Prostaglandins are synthesized from arachidonic acid, a polyunsaturated fatty acid derived from membrane phospholipids, by the action of cyclooxygenase (COX) enzymes. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin and ibuprofen, inhibit COX activity, reducing prostaglandin synthesis and providing analgesic, anti-inflammatory, and antipyretic effects.

Peroxides, in a medical context, most commonly refer to chemical compounds that contain the peroxide ion (O2−2). Peroxides are characterized by the presence of an oxygen-oxygen single bond and can be found in various substances.

In dentistry, hydrogen peroxide (H2O2) is a widely used agent for teeth whitening or bleaching due to its oxidizing properties. It can help remove stains and discoloration on the tooth surface by breaking down into water and oxygen-free radicals, which react with the stain molecules, ultimately leading to their oxidation and elimination.

However, it is essential to note that high concentrations of hydrogen peroxide or prolonged exposure can cause tooth sensitivity, irritation to the oral soft tissues, and potential damage to the dental pulp. Therefore, professional supervision and appropriate concentration control are crucial when using peroxides for dental treatments.

Prostaglandin H2 (PGH2) is not a medical condition, but rather a chemical compound that acts as a precursor in the synthesis of other prostaglandins and thromboxanes. It is produced from arachidonic acid by the action of the enzyme cyclooxygenase (COX). PGH2 is then converted into various downstream prostanoids, such as PGD2, PGE2, PGF2α, PGI2 (prostacyclin), and TXA2 (thromboxane A2), by specific synthases. These prostanoids have diverse biological activities, including regulation of inflammation, pain, fever, blood flow, and platelet aggregation.

Thromboxane-A Synthase (TXA2S) is a medical term referring to an enzyme that plays a crucial role in the blood coagulation process. It is found in platelets, and its primary function is to convert arachidonic acid into thromboxane A2 (TXA2), a potent vasoconstrictor and platelet aggregator.

Thromboxane A2 causes platelets to clump together, which is essential for the formation of blood clots that can help prevent excessive bleeding after an injury. However, an overproduction of thromboxane A2 can lead to the development of blood clots in blood vessels, increasing the risk of heart attack and stroke.

Therefore, Thromboxane-A Synthase is a vital enzyme in hemostasis (the process that stops bleeding), but its dysregulation can contribute to various cardiovascular diseases.

Dibenzothiepins are a class of chemical compounds that contain a dibenzothiepin ring structure. This ring structure is composed of two benzene rings fused to a thiepin ring, which is a six-membered ring containing a sulfur atom and a double bond.

In the medical field, dibenzothiepins are primarily known for their use as antipsychotic drugs. The first dibenzothiepin antipsychotic, clopenthixol, was synthesized in the 1960s and found to have potent antipsychotic effects. Since then, several other dibenzothiepins have been developed for use as antipsychotics, including flupentixol and thiothixene.

These drugs work by blocking dopamine receptors in the brain, which helps to reduce the symptoms of psychosis such as hallucinations, delusions, and disorganized thinking. However, they can also cause side effects such as extrapyramidal symptoms (involuntary muscle movements), sedation, and weight gain.

It's worth noting that while dibenzothiepins have been used as antipsychotics for several decades, they are not commonly prescribed today due to the availability of newer antipsychotic drugs with fewer side effects.

Prostaglandin E (PGE) is a type of prostaglandin, which is a group of lipid compounds that are synthesized in the body from fatty acids and have diverse hormone-like effects. Prostaglandins are not actually hormones, but are similar to them in that they act as chemical messengers that have specific effects on certain cells.

Prostaglandin E is one of the most abundant prostaglandins in the body and has a variety of physiological functions. It is involved in the regulation of inflammation, pain perception, fever, and smooth muscle contraction. Prostaglandin E also plays a role in the regulation of blood flow, platelet aggregation, and gastric acid secretion.

Prostaglandin E is synthesized from arachidonic acid, which is released from cell membranes by the action of enzymes called phospholipases. Once formed, prostaglandin E binds to specific receptors on the surface of cells, leading to a variety of intracellular signaling events that ultimately result in changes in cell behavior.

Prostaglandin E is used medically in the treatment of several conditions, including dysmenorrhea (painful menstruation), postpartum hemorrhage, and patent ductus arteriosus (a congenital heart defect). It is also used as a diagnostic tool in the evaluation of kidney function.

Synthetic prostaglandins are human-made versions of prostaglandins, which are naturally occurring hormone-like substances in the body that play many roles in health and disease. Prostaglandins are produced in various tissues throughout the body and have diverse effects, such as regulating blood flow, promoting inflammation, causing muscle contraction or relaxation, and modulating pain perception.

Synthetic prostaglandins are developed to mimic the effects of natural prostaglandins and are used for therapeutic purposes in medical treatments. They can be chemically synthesized or derived from animal tissues. Synthetic prostaglandins have been used in various clinical settings, including:

1. Induction of labor: Synthetic prostaglandin E1 (dinoprostone) and prostaglandin E2 (misoprostol) are used to ripen the cervix and induce labor in pregnant women.
2. Abortion: Misoprostol is used off-label for early pregnancy termination, often in combination with mifepristone.
3. Prevention of nonsteroidal anti-inflammatory drug (NSAID)-induced gastric ulcers: Misoprostol is sometimes prescribed to protect the stomach lining from developing ulcers due to long-term NSAID use.
4. Treatment of postpartum hemorrhage: Synthetic prostaglandins like carboprost (15-methyl prostaglandin F2α) and dinoprostone are used to manage severe bleeding after childbirth.
5. Management of dysmenorrhea: Misoprostol is sometimes prescribed for the treatment of painful periods or menstrual cramps.
6. Treatment of erectile dysfunction: Alprostadil, a synthetic prostaglandin E1, can be used as an intracavernosal injection or urethral suppository to treat erectile dysfunction.

It is important to note that while synthetic prostaglandins mimic the effects of natural prostaglandins, they may also have additional or different properties and potential side effects. Therefore, their use should be under the guidance and supervision of a healthcare professional.

The seminal vesicles are a pair of glands located in the male reproductive system, posterior to the urinary bladder and superior to the prostate gland. They are approximately 5 cm long and have a convoluted structure with many finger-like projections called infoldings. The primary function of seminal vesicles is to produce and secrete a significant portion of the seminal fluid, which makes up the bulk of semen along with spermatozoa from the testes and fluids from the prostate gland and bulbourethral glands.

The secretion of the seminal vesicles is rich in fructose, which serves as an energy source for sperm, as well as various proteins, enzymes, vitamins, and minerals that contribute to maintaining the optimal environment for sperm survival, nourishment, and transport. During sexual arousal and ejaculation, the smooth muscles in the walls of the seminal vesicles contract, forcing the stored secretion into the urethra, where it mixes with other fluids before being expelled from the body as semen.

Arachidonic acids are a type of polyunsaturated fatty acid that is primarily found in the phospholipids of cell membranes. They contain 20 carbon atoms and four double bonds (20:4n-6), with the first double bond located at the sixth carbon atom from the methyl end.

Arachidonic acids are derived from linoleic acid, an essential fatty acid that cannot be synthesized by the human body and must be obtained through dietary sources such as meat, fish, and eggs. Once ingested, linoleic acid is converted to arachidonic acid in a series of enzymatic reactions.

Arachidonic acids play an important role in various physiological processes, including inflammation, immune response, and cell signaling. They serve as precursors for the synthesis of eicosanoids, which are signaling molecules that include prostaglandins, thromboxanes, and leukotrienes. These eicosanoids have diverse biological activities, such as modulating blood flow, platelet aggregation, and pain perception, among others.

However, excessive production of arachidonic acid-derived eicosanoids has been implicated in various pathological conditions, including inflammation, atherosclerosis, and cancer. Therefore, the regulation of arachidonic acid metabolism is an important area of research for the development of new therapeutic strategies.

Hydrazines are not a medical term, but rather a class of organic compounds containing the functional group N-NH2. They are used in various industrial and chemical applications, including the production of polymers, pharmaceuticals, and agrochemicals. However, some hydrazines have been studied for their potential therapeutic uses, such as in the treatment of cancer and cardiovascular diseases. Exposure to high levels of hydrazines can be toxic and may cause damage to the liver, kidneys, and central nervous system. Therefore, medical professionals should be aware of the potential health hazards associated with hydrazine exposure.

Thromboxane receptors are a type of G protein-coupled receptor that binds thromboxane A2 (TXA2), a powerful inflammatory mediator and vasoconstrictor synthesized in the body from arachidonic acid. These receptors play a crucial role in various physiological processes, including platelet aggregation, smooth muscle contraction, and modulation of immune responses.

There are two main types of thromboxane receptors: TPα and TPβ. The TPα receptor is primarily found on platelets and vascular smooth muscle cells, while the TPβ receptor is expressed in various tissues such as the kidney, lung, and brain. Activation of these receptors by thromboxane A2 leads to a variety of cellular responses, including platelet activation and aggregation, vasoconstriction, and inflammation.

Abnormalities in thromboxane receptor function have been implicated in several pathological conditions, such as cardiovascular diseases, asthma, and cancer. Therefore, thromboxane receptors are an important target for the development of therapeutic agents to treat these disorders.

Hydroxy acids are a class of chemical compounds that contain both a carboxylic acid group and a hydroxyl group. They are commonly used in dermatology and cosmetic products for their exfoliating, moisturizing, and anti-aging properties. The two main types of hydroxy acids used in skincare are alpha-hydroxy acids (AHAs) and beta-hydroxy acids (BHAs).

Alpha-hydroxy acids include compounds such as glycolic acid, lactic acid, malic acid, tartaric acid, and citric acid. They work by breaking down the "glue" that holds dead skin cells together, promoting cell turnover and helping to improve the texture and tone of the skin. AHAs are also known for their ability to improve the appearance of fine lines, wrinkles, and age spots.

Beta-hydroxy acids, on the other hand, are primarily represented by salicylic acid. BHAs are oil-soluble, which allows them to penetrate deeper into the pores and exfoliate dead skin cells and excess sebum that can lead to clogged pores and acne breakouts.

It is important to note that hydroxy acids can cause skin irritation and sensitivity to sunlight, so it is recommended to use sunscreen and start with lower concentrations when first incorporating them into a skincare routine.

Platelet aggregation is the clumping together of platelets (thrombocytes) in the blood, which is an essential step in the process of hemostasis (the stopping of bleeding) after injury to a blood vessel. When the inner lining of a blood vessel is damaged, exposure of subendothelial collagen and tissue factor triggers platelet activation. Activated platelets change shape, become sticky, and release the contents of their granules, which include ADP (adenosine diphosphate).

ADP then acts as a chemical mediator to attract and bind additional platelets to the site of injury, leading to platelet aggregation. This forms a plug that seals the damaged vessel and prevents further blood loss. Platelet aggregation is also a crucial component in the formation of blood clots (thrombosis) within blood vessels, which can have pathological consequences such as heart attacks and strokes if they obstruct blood flow to vital organs.

Thromboxane B2 (TXB2) is a stable metabolite of thromboxane A2 (TXA2), which is a potent vasoconstrictor and platelet aggregator synthesized by activated platelets. TXA2 has a very short half-life, quickly undergoing spontaneous conversion to the more stable TXB2.

TXB2 itself does not have significant biological activity but serves as a marker for TXA2 production in various physiological and pathophysiological conditions, such as thrombosis, inflammation, and atherosclerosis. It can be measured in blood or other bodily fluids to assess platelet activation and the status of hemostatic and inflammatory processes.

Thromboxane A2 (TXA2) is a potent prostanoid, a type of lipid compound derived from arachidonic acid. It is primarily produced and released by platelets upon activation during the process of hemostasis (the body's response to stop bleeding). TXA2 acts as a powerful vasoconstrictor, causing blood vessels to narrow, which helps limit blood loss at the site of injury. Additionally, it promotes platelet aggregation, contributing to the formation of a stable clot and preventing further bleeding. However, uncontrolled or excessive production of TXA2 can lead to thrombotic events such as heart attacks and strokes. Its effects are balanced by prostacyclin (PGI2), which is produced by endothelial cells and has opposing actions, acting as a vasodilator and inhibiting platelet aggregation. The balance between TXA2 and PGI2 helps maintain vascular homeostasis.

Thromboxanes are a type of lipid compound that is derived from arachidonic acid, a type of fatty acid found in the cell membranes of many organisms. They are synthesized in the body through the action of an enzyme called cyclooxygenase (COX).

Thromboxanes are primarily produced by platelets, a type of blood cell that plays a key role in clotting. Once formed, thromboxanes act as powerful vasoconstrictors, causing blood vessels to narrow and blood flow to decrease. They also promote the aggregation of platelets, which can lead to the formation of blood clots.

Thromboxanes are involved in many physiological processes, including hemostasis (the process by which bleeding is stopped) and inflammation. However, excessive production of thromboxanes has been implicated in a number of pathological conditions, such as heart attacks, strokes, and pulmonary hypertension.

There are several different types of thromboxanes, including thromboxane A2 (TXA2) and thromboxane B2 (TXB2). TXA2 is the most biologically active form and has a very short half-life, while TXB2 is a more stable metabolite that can be measured in the blood to assess thromboxane production.

Prostaglandin F (PGF) is a type of prostaglandin, which is a group of lipid compounds that are synthesized in the body from fatty acids and have diverse hormone-like effects. Prostaglandin F is a naturally occurring compound that is produced in various tissues throughout the body, including the uterus, lungs, and kidneys.

There are two major types of prostaglandin F: PGF1α and PGF2α. These compounds play important roles in a variety of physiological processes, including:

* Uterine contraction: Prostaglandin F helps to stimulate uterine contractions during labor and childbirth. It is also involved in the shedding of the uterine lining during menstruation.
* Bronchodilation: In the lungs, prostaglandin F can help to relax bronchial smooth muscle and promote bronchodilation.
* Renal function: Prostaglandin F helps to regulate blood flow and fluid balance in the kidneys.

Prostaglandin F is also used as a medication to induce labor, treat postpartum hemorrhage, and manage some types of glaucoma. It is available in various forms, including injections, tablets, and eye drops.

Indomethacin is a non-steroidal anti-inflammatory drug (NSAID) that is commonly used to reduce pain, inflammation, and fever. It works by inhibiting the activity of certain enzymes in the body, including cyclooxygenase (COX), which plays a role in producing prostaglandins, chemicals involved in the inflammatory response.

Indomethacin is available in various forms, such as capsules, suppositories, and injectable solutions, and is used to treat a wide range of conditions, including rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, gout, and bursitis. It may also be used to relieve pain and reduce fever in other conditions, such as dental procedures or after surgery.

Like all NSAIDs, indomethacin can have side effects, including stomach ulcers, bleeding, and kidney damage, especially when taken at high doses or for long periods of time. It may also increase the risk of heart attack and stroke. Therefore, it is important to use indomethacin only as directed by a healthcare provider and to report any unusual symptoms or side effects promptly.

Blood platelets, also known as thrombocytes, are small, colorless cell fragments in our blood that play an essential role in normal blood clotting. They are formed in the bone marrow from large cells called megakaryocytes and circulate in the blood in an inactive state until they are needed to help stop bleeding. When a blood vessel is damaged, platelets become activated and change shape, releasing chemicals that attract more platelets to the site of injury. These activated platelets then stick together to form a plug, or clot, that seals the wound and prevents further blood loss. In addition to their role in clotting, platelets also help to promote healing by releasing growth factors that stimulate the growth of new tissue.

Prostaglandin receptors are a type of cell surface receptor that bind and respond to prostaglandins, which are hormone-like lipid compounds that play important roles in various physiological and pathophysiological processes in the body. Prostaglandins are synthesized from arachidonic acid by the action of enzymes called cyclooxygenases (COX) and are released by many different cell types in response to various stimuli.

There are four major subfamilies of prostaglandin receptors, designated as DP, EP, FP, and IP, each of which binds specifically to one or more prostaglandins with high affinity. These receptors are G protein-coupled receptors (GPCRs), which means that they activate intracellular signaling pathways through the interaction with heterotrimeric G proteins.

The activation of prostaglandin receptors can lead to a variety of cellular responses, including changes in ion channel activity, enzyme activation, and gene expression. These responses can have important consequences for many physiological processes, such as inflammation, pain perception, blood flow regulation, and platelet aggregation.

Prostaglandin receptors are also targets for various drugs used in clinical medicine, including nonsteroidal anti-inflammatory drugs (NSAIDs) and prostaglandin analogs. NSAIDs work by inhibiting the enzymes that synthesize prostaglandins, while prostaglandin analogs are synthetic compounds that mimic the effects of natural prostaglandins by activating specific prostaglandin receptors.

In summary, prostaglandin receptors are a class of cell surface receptors that bind and respond to prostaglandins, which are important signaling molecules involved in various physiological processes. These receptors are targets for various drugs used in clinical medicine and play a critical role in the regulation of many bodily functions.

Dinoprostone is a prostaglandin E2 analog used in medical practice for the induction of labor and ripening of the cervix in pregnant women. It is available in various forms, including vaginal suppositories, gel, and tablets. Dinoprostone works by stimulating the contraction of uterine muscles and promoting cervical dilation, which helps in facilitating a successful delivery.

It's important to note that dinoprostone should only be administered under the supervision of a healthcare professional, as its use is associated with certain risks and side effects, including uterine hyperstimulation, fetal distress, and maternal infection. The dosage and duration of treatment are carefully monitored to minimize these risks and ensure the safety of both the mother and the baby.

Prostaglandin D2 (PGD2) is a type of prostaglandin, which is a group of lipid compounds that are derived enzymatically from arachidonic acid and have diverse hormone-like effects in various tissues. PGD2 is one of the most abundant prostaglandins produced in the human body and is primarily synthesized and released by activated mast cells, which are a type of immune cell found in various tissues throughout the body.

PGD2 has a wide range of biological activities, including vasodilation, bronchoconstriction, and modulation of immune responses. It also plays important roles in regulating sleep and wakefulness, as well as in the development of allergic inflammation and other inflammatory processes. PGD2 exerts its effects by binding to specific G protein-coupled receptors, including the DP1 and CRTH2 receptors, which are expressed on various cell types throughout the body.

In addition to its role in normal physiological processes, PGD2 has also been implicated in a number of pathological conditions, including asthma, rhinitis, dermatitis, and certain types of cancer. As such, drugs that target the synthesis or action of PGD2 have been developed as potential therapeutic agents for these conditions.

I'm sorry for any confusion, but there is no such thing as "Prostaglandins A." Prostaglandins are a group of lipid compounds that are derived enzymatically from fatty acids in the body, and they have diverse hormone-like effects in various tissues. They are typically classified into several groups based on their chemical structure, including prostaglandin D, E, F, I, and THC (tetrahydrocannabinol). Prostaglandin A is not a recognized subtype of prostaglandins.

If you have any questions about a specific type of prostaglandin or another medical topic, please don't hesitate to ask!

Prostaglandin-Endoperoxide Synthases (PTGS), also known as Cyclooxygenases (COX), are a group of enzymes that catalyze the conversion of arachidonic acid into prostaglandin G2 and H2, which are further metabolized to produce various prostaglandins and thromboxanes. These lipid mediators play crucial roles in several physiological processes such as inflammation, pain, fever, and blood clotting. There are two major isoforms of PTGS: PTGS-1 (COX-1) and PTGS-2 (COX-2). While COX-1 is constitutively expressed in most tissues and involved in homeostatic functions, COX-2 is usually induced during inflammation and tissue injury. Nonsteroidal anti-inflammatory drugs (NSAIDs) exert their therapeutic effects by inhibiting these enzymes, thereby reducing the production of prostaglandins and thromboxanes.

Prostaglandin E (PGE) receptors are a type of G protein-coupled receptor that bind and respond to prostaglandin E, a group of lipid compounds called eicosanoids that have various hormone-like effects in the body. PGE receptors play important roles in regulating numerous physiological processes, including inflammation, pain perception, fever, gastrointestinal motility and mucosal protection, blood flow, and labor and delivery.

There are four subtypes of PGE receptors, designated EP1, EP2, EP3, and EP4, each with distinct signaling pathways and functions. For example, activation of EP1 receptors can increase calcium levels in cells and promote pain sensation, while activation of EP2 and EP4 receptors can stimulate the production of cyclic AMP (cAMP) and have anti-inflammatory effects. EP3 receptors can have both excitatory and inhibitory effects on cellular signaling, depending on the specific isoform and downstream signaling pathways involved.

Abnormalities in PGE receptor function or expression have been implicated in various disease states, including inflammatory disorders, pain syndromes, cardiovascular diseases, and cancer. As a result, PGE receptors are an active area of research for the development of new therapeutic strategies to target these conditions.

Prostaglandin antagonists are a class of medications that work by blocking the action of prostaglandins, which are hormone-like substances that play many roles in the body, including causing inflammation, promoting uterine contractions during labor and menstruation, and regulating blood flow in various tissues.

Prostaglandin antagonists are often used to treat conditions that involve excessive prostaglandin activity, such as:

* Pain and inflammation associated with arthritis or musculoskeletal injuries
* Migraines and other headaches
* Dysmenorrhea (painful menstruation)
* Preterm labor

Examples of prostaglandin antagonists include nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen, naproxen, and celecoxib, as well as specific prostaglandin receptor antagonists such as misoprostol and telmisartan.

It's important to note that while prostaglandin antagonists can be effective in treating certain conditions, they can also have side effects and potential risks, so it's important to use them under the guidance of a healthcare provider.

I am sorry for any confusion, but "Pentanoic Acids" is not a recognized medical term or concept. Pentanoic acid, also known as valeric acid, is an organic compound with the formula CH3CH2CH2CH2CO2H. It is a fatty acid with five carbon atoms, and it may have some uses in industry, but it does not have specific relevance to medical definition or healthcare.

I'm sorry for any confusion, but "Prostaglandins D" is not a recognized or established term in the field of medicine or physiology. Prostaglandins are a group of lipid compounds that are synthesized in the body from fatty acids and have diverse hormone-like effects in the body. They are classified into several types based on their chemical structure and biological activity, including Prostaglandin D (PGD), but referring to "Prostaglandins D" as a single entity is not standard.

Prostaglandin D (PGD) itself is a type of prostaglandin that is rapidly converted to other compounds in the body and has been studied for its potential role in various physiological processes, such as inflammation, fever, and blood flow regulation. However, it's important to note that specific medical definitions or clinical uses related to "Prostaglandins D" are not well-established.

If you have any further questions or need more information about a specific aspect of prostaglandins or their role in the body, I would be happy to help!

Epoprostenol is a medication that belongs to a class of drugs called prostaglandins. It is a synthetic analog of a natural substance in the body called prostacyclin, which widens blood vessels and has anti-platelet effects. Epoprostenol is used to treat pulmonary arterial hypertension (PAH), a condition characterized by high blood pressure in the arteries that supply blood to the lungs.

Epoprostenol works by relaxing the smooth muscle in the walls of the pulmonary arteries, which reduces the resistance to blood flow and lowers the pressure within these vessels. This helps improve symptoms such as shortness of breath, fatigue, and chest pain, and can also prolong survival in people with PAH.

Epoprostenol is administered continuously through a small pump that delivers the medication directly into the bloodstream. It is a potent vasodilator, which means it can cause a sudden drop in blood pressure if not given carefully. Therefore, it is usually started in a hospital setting under close medical supervision.

Common side effects of epoprostenol include headache, flushing, jaw pain, nausea, vomiting, diarrhea, and muscle or joint pain. More serious side effects can include bleeding, infection at the site of the catheter, and an allergic reaction to the medication.

Prostaglandin E (PGE) receptors are a type of G protein-coupled receptor that bind and respond to prostaglandin E, a lipid mediator involved in various physiological processes such as inflammation, pain perception, and fever. The EP4 subtype is one of four known subtypes of PGE receptors (EP1-EP4) and is encoded by the PTGER4 gene in humans.

The EP4 receptor is widely expressed in various tissues, including the cardiovascular system, gastrointestinal tract, and central nervous system. It plays a crucial role in several physiological functions, such as vasodilation, platelet aggregation, and immune response regulation. In addition, EP4 activation has been implicated in pathophysiological processes, including cancer progression, chronic pain, and inflammatory diseases.

EP4 receptors activate various downstream signaling pathways upon binding to PGE, such as the adenylyl cyclase/cAMP pathway, which leads to increased intracellular cAMP levels and protein kinase A (PKA) activation. This results in the phosphorylation of several target proteins involved in cell proliferation, survival, and migration.

Overall, Prostaglandin E receptors, EP4 subtype, are essential mediators of various physiological and pathophysiological processes, making them an attractive therapeutic target for various diseases.

Arachidonic acid is a type of polyunsaturated fatty acid that is found naturally in the body and in certain foods. It is an essential fatty acid, meaning that it cannot be produced by the human body and must be obtained through the diet. Arachidonic acid is a key component of cell membranes and plays a role in various physiological processes, including inflammation and blood clotting.

In the body, arachidonic acid is released from cell membranes in response to various stimuli, such as injury or infection. Once released, it can be converted into a variety of bioactive compounds, including prostaglandins, thromboxanes, and leukotrienes, which mediate various physiological responses, including inflammation, pain, fever, and blood clotting.

Arachidonic acid is found in high concentrations in animal products such as meat, poultry, fish, and eggs, as well as in some plant sources such as certain nuts and seeds. It is also available as a dietary supplement. However, it is important to note that excessive intake of arachidonic acid can contribute to the development of inflammation and other health problems, so it is recommended to consume this fatty acid in moderation as part of a balanced diet.

Prostaglandin E (PGE) receptors are a type of G protein-coupled receptor that bind and respond to prostaglandin E, a lipid mediator involved in various physiological processes such as inflammation, pain perception, and fever. There are four subtypes of PGE receptors, designated EP1, EP2, EP3, and EP4.

The EP2 subtype of PGE receptor is a G protein-coupled receptor that specifically binds to prostaglandin E2 (PGE2) and activates the Gs protein, leading to an increase in intracellular cyclic AMP (cAMP) levels. The activation of EP2 receptors has been shown to have various effects on different tissues, including vasodilation, bronchodilation, and inhibition of platelet aggregation. In addition, EP2 receptors are involved in pain perception, inflammation, and neuroprotection.

EP2 receptors are widely expressed in the body, including in the brain, spinal cord, heart, lungs, gastrointestinal tract, and reproductive organs. They play a crucial role in various physiological processes, such as regulating blood flow, modulating immune responses, and controlling smooth muscle contraction. Dysregulation of EP2 receptor signaling has been implicated in several pathological conditions, including inflammatory diseases, pain disorders, and cancer.

Dinoprost is a synthetic form of prostaglandin F2α, which is a naturally occurring hormone-like substance in the body. It is used in veterinary medicine as a uterotonic agent to induce labor and abortion in various animals such as cows and pigs. In human medicine, it may be used off-label for similar purposes, but its use must be under the close supervision of a healthcare provider due to potential side effects and risks.

It is important to note that Dinoprost is not approved by the FDA for use in humans, and its availability may vary depending on the country or region. Always consult with a licensed healthcare professional before using any medication, including Dinoprost.

Alprostadil is a synthetic form of prostaglandin E1, which is a naturally occurring substance in the body. It is used medically for several purposes, including:

1. Treatment of erectile dysfunction (ED): Alprostadil can be administered directly into the penis as an injection or inserted as a suppository into the urethra to help improve blood flow and achieve an erection.
2. Prevention of closure of a patent ductus arteriosus (PDA) in premature infants: Alprostadil is used to keep the PDA open, allowing for proper blood flow between the pulmonary artery and the aorta, until surgery can be performed.
3. Treatment of peripheral arterial disease: Alprostadil can be administered intravenously to help improve blood flow in patients with peripheral arterial disease.

Alprostadil works by relaxing smooth muscle tissue in blood vessels, which increases blood flow and helps to lower blood pressure. It may also have other effects on the body, such as reducing the risk of blood clots and modulating inflammation.

It is important to note that alprostadil should only be used under the supervision of a healthcare provider, as it can have serious side effects if not used properly.

Prostaglandin E (PGE) receptors are a subfamily of G protein-coupled receptors that are involved in various physiological and pathophysiological processes. The EP1 subtype of PGE receptors is one of four subtypes, along with EP2, EP3, and EP4.

EP1 receptors are widely expressed in various tissues, including the brain, heart, kidney, lung, and gastrointestinal tract. They are coupled to Gq proteins, which activate phospholipase C (PLC) and increase intracellular calcium levels upon activation.

EP1 receptor activation has been implicated in a variety of physiological responses, including vasoconstriction, increased heart rate and contractility, and inflammation. In the central nervous system, EP1 receptors have been shown to play a role in pain perception, thermoregulation, and neuroprotection.

Pharmacologically, selective EP1 receptor antagonists have been developed and are being investigated for their potential therapeutic benefits in various conditions, such as hypertension, myocardial ischemia, and inflammatory diseases.

Prostaglandins E, Synthetic are a class of medications that mimic the effects of natural prostaglandins, which are hormone-like substances involved in various bodily functions, including inflammation, pain perception, and regulation of the female reproductive system. Prostaglandin E1 (PGE1) is one of the most commonly synthesized prostaglandins used in medical treatments.

Synthetic prostaglandins E are often used for their vasodilatory effects, which help to improve blood flow and reduce blood pressure. They may also be used to prevent or treat blood clots, as well as to manage certain conditions related to the female reproductive system, such as inducing labor or causing an abortion.

Some examples of synthetic prostaglandins E include misoprostol (Cytotec), dinoprostone (Cervidil, Prepidil), and alprostadil (Edex, Caverject). These medications are available in various forms, such as tablets, suppositories, or injectable solutions, and their use depends on the specific medical condition being treated.

It is important to note that synthetic prostaglandins E can have significant side effects, including gastrointestinal symptoms (such as diarrhea, nausea, and vomiting), abdominal pain, and uterine contractions. Therefore, they should only be used under the close supervision of a healthcare provider.

Microsomes are subcellular membranous vesicles that are obtained as a byproduct during the preparation of cellular homogenates. They are not naturally occurring structures within the cell, but rather formed due to fragmentation of the endoplasmic reticulum (ER) during laboratory procedures. Microsomes are widely used in various research and scientific studies, particularly in the fields of biochemistry and pharmacology.

Microsomes are rich in enzymes, including the cytochrome P450 system, which is involved in the metabolism of drugs, toxins, and other xenobiotics. These enzymes play a crucial role in detoxifying foreign substances and eliminating them from the body. As such, microsomes serve as an essential tool for studying drug metabolism, toxicity, and interactions, allowing researchers to better understand and predict the effects of various compounds on living organisms.

Prostaglandin E (PGE) receptors are a type of G protein-coupled receptor that bind and respond to prostaglandin E, a lipid mediator involved in various physiological processes such as inflammation, pain perception, and smooth muscle contraction. The EP3 subtype is one of four subtypes of PGE receptors (EP1-EP4) and has been identified as playing a role in several important biological functions.

The EP3 receptor is widely expressed in various tissues, including the brain, heart, lungs, gastrointestinal tract, and reproductive organs. It can couple with multiple G proteins, leading to diverse downstream signaling pathways that regulate a range of cellular responses. The activation of EP3 receptors has been implicated in several physiological processes, such as:

1. Modulation of pain perception and inflammation: EP3 receptors can inhibit the release of pro-inflammatory cytokines and chemokines, which may contribute to their anti-inflammatory effects. However, they can also promote the production of other mediators that enhance pain signaling, making them a potential target for pain management therapies.
2. Regulation of smooth muscle contraction: EP3 receptors are involved in the regulation of smooth muscle tone in various organs, including the gastrointestinal tract and blood vessels. They can cause relaxation or contraction depending on the specific tissue and context.
3. Control of hormone secretion: EP3 receptors have been shown to regulate the release of several hormones, such as insulin, glucagon, and gonadotropins, which play crucial roles in metabolic homeostasis and reproduction.
4. Neuroprotection and neuroinflammation: In the central nervous system, EP3 receptors can have both neuroprotective and neurotoxic effects, depending on the context. They may contribute to the regulation of neuroinflammation and the development of certain neurological disorders.
5. Cardiovascular function: EP3 receptors are involved in the regulation of cardiovascular function, including blood pressure control and heart rate modulation.

Due to their diverse roles in various physiological processes, EP3 receptors have attracted significant interest as potential therapeutic targets for a wide range of diseases, such as inflammatory disorders, pain management, gastrointestinal dysfunction, metabolic disorders, and neurological conditions. However, further research is needed to fully understand their mechanisms of action and develop effective strategies for targeting them in clinical settings.

Aspirin is the common name for acetylsalicylic acid, which is a medication used to relieve pain, reduce inflammation, and lower fever. It works by inhibiting the activity of an enzyme called cyclooxygenase (COX), which is involved in the production of prostaglandins, hormone-like substances that cause inflammation and pain. Aspirin also has an antiplatelet effect, which means it can help prevent blood clots from forming. This makes it useful for preventing heart attacks and strokes.

Aspirin is available over-the-counter in various forms, including tablets, capsules, and chewable tablets. It is also available in prescription strengths for certain medical conditions. As with any medication, aspirin should be taken as directed by a healthcare provider, and its use should be avoided in children and teenagers with viral infections due to the risk of Reye's syndrome, a rare but serious condition that can affect the liver and brain.

Cyclooxygenase-2 (COX-2) is an enzyme involved in the synthesis of prostaglandins, which are hormone-like substances that play a role in inflammation, pain, and fever. COX-2 is primarily expressed in response to stimuli such as cytokines and growth factors, and its expression is associated with the development of inflammation.

COX-2 inhibitors are a class of nonsteroidal anti-inflammatory drugs (NSAIDs) that selectively block the activity of COX-2, reducing the production of prostaglandins and providing analgesic, anti-inflammatory, and antipyretic effects. These medications are often used to treat pain and inflammation associated with conditions such as arthritis, menstrual cramps, and headaches.

It's important to note that while COX-2 inhibitors can be effective in managing pain and inflammation, they may also increase the risk of cardiovascular events such as heart attack and stroke, particularly when used at high doses or for extended periods. Therefore, it's essential to use these medications under the guidance of a healthcare provider and to follow their instructions carefully.

Artemisinins are a class of antimalarial drugs derived from the sweet wormwood plant (Artemisia annua). They are highly effective against Plasmodium falciparum, the most deadly species of malaria parasite. Artemisinins have become an essential component in the treatment of malaria and are often used in combination therapy regimens to reduce the risk of drug resistance.

The artemisinin compounds contain a unique peroxide bridge that is responsible for their antimalarial activity. They work by generating free radicals that can damage the parasite's membranes, leading to its rapid death. Artemisinins have a fast action and can significantly reduce the parasite biomass in the first few days of treatment.

Some commonly used artemisinin-based combination therapies (ACTs) include:

* Artemether-lumefantrine (Coartem)
* Artesunate-amodiaquine (Coarsucam)
* Artesunate-mefloquine (Artequin)
* Dihydroartemisinin-piperaquine (Eurartesim, Duo-Cotecxin)

Artemisinins have also shown potential in treating other conditions, such as certain types of cancer and viral infections. However, more research is needed to establish their safety and efficacy for these indications.

Thin-layer chromatography (TLC) is a type of chromatography used to separate, identify, and quantify the components of a mixture. In TLC, the sample is applied as a small spot onto a thin layer of adsorbent material, such as silica gel or alumina, which is coated on a flat, rigid support like a glass plate. The plate is then placed in a developing chamber containing a mobile phase, typically a mixture of solvents.

As the mobile phase moves up the plate by capillary action, it interacts with the stationary phase and the components of the sample. Different components of the mixture travel at different rates due to their varying interactions with the stationary and mobile phases, resulting in distinct spots on the plate. The distance each component travels can be measured and compared to known standards to identify and quantify the components of the mixture.

TLC is a simple, rapid, and cost-effective technique that is widely used in various fields, including forensics, pharmaceuticals, and research laboratories. It allows for the separation and analysis of complex mixtures with high resolution and sensitivity, making it an essential tool in many analytical applications.

Intramolecular oxidoreductases are a specific class of enzymes that catalyze the transfer of electrons within a single molecule, hence the term "intramolecular." These enzymes are involved in oxidoreduction reactions, where one part of the molecule is oxidized (loses electrons) and another part is reduced (gains electrons). This process allows for the rearrangement or modification of functional groups within the molecule.

The term "oxidoreductase" refers to enzymes that catalyze oxidation-reduction reactions, which are also known as redox reactions. These enzymes play a crucial role in various biological processes, including energy metabolism, detoxification, and biosynthesis.

It's important to note that intramolecular oxidoreductases should not be confused with intermolecular oxidoreductases, which catalyze redox reactions between two separate molecules.

... is a stable synthetic analog of the endoperoxide prostaglandin PGH2 first prepared in 1975, and acts as a thromboxane A2 ... Bundy, G. L. (1975). "Synthesis of prostaglandin endoperoxide analogs". Tetrahedron Letters. 16 (24): 1957-1960. doi:10.1016/ ... It potently stimulates TP receptor-mediated, but not other prostaglandin receptor-mediated responses in various in vitro ... S0040-4039(00)72333-1. Liel, N.; Mais, D.E.; Halushka, P.V (1987). "Binding of a thromboxane A2/prostaglandin H2 agonist [3H] ...
... prostaglandin endoperoxides, synthetic MeSH D10.251.355.255.550.700.350 - prostaglandins a, synthetic MeSH D10.251.355.255. ... prostaglandins MeSH D10.251.355.255.550.025 - prostaglandin endoperoxides MeSH D10.251.355.255.550.025.600 - prostaglandins g ... prostaglandins i MeSH D10.251.355.255.550.550.500 - epoprostenol MeSH D10.251.355.255.550.700 - prostaglandins, synthetic MeSH ... prostaglandin endoperoxides MeSH D10.251.355.255.100.637.025.600 - prostaglandins g MeSH D10.251.355.255.100.637.025.650 - ...
... prostaglandin endoperoxides, synthetic MeSH D23.469.700.630.500 - 15-hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic ... prostaglandins MeSH D23.469.050.175.725.720 - prostaglandin endoperoxides MeSH D23.469.050.175.725.720.700 - prostaglandins g ... acid MeSH D23.469.700.645 - prostaglandins a, synthetic MeSH D23.469.700.660 - prostaglandins e, synthetic MeSH D23.469.700.660 ... prostaglandins a MeSH D23.469.050.175.725.750 - prostaglandins b MeSH D23.469.050.175.725.770 - prostaglandins d MeSH D23.469. ...
Hamberg, M; Samuelsson, B (1974). "Prostaglandin endoperoxides. Novel transformations of arachidonic acid in human platelets". ... Synthetic BLT2 agonists may be useful for speeding the healing of chronic ulcerative wounds, particularly in patients with, for ... "Xenobiotic-metabolizing cytochromes P450 convert prostaglandin endoperoxide to hydroxyheptadecatrienoic acid and the mutagen, ... Prostaglandin E2 and Prostaglandin D2, but not 12 other lipoxygenase or cycloxygenase metabolites, showed a statistically ...
In platelets this fatty acid is metabolized to an endoperoxide called prostaglandin H2 by the enzyme cyclooxygenase 1. This ... but a complete synthetic proposal was made to indicate the synthetic options. Only one form of furegrelate is commercially ... Furegrelate is a synthetic compound that cannot be synthesised by the human body. Several pathways were proposed for the ... It does this presumably by enhancing the formation of vasodilator prostaglandins. Inhibition of furegrelate induced a ...
Many sensitizers, both naturally occurring and synthetic, rely on extensive aromatic systems to absorb light in the visible ... A Simple, Stereocontrolled Route to Prostaglandin Fza". J. Am. Chem. Soc. 108 (20): 6384-6385. doi:10.1021/ja00280a043. Li, Yun ... The initial addition singlet oxygen, through the concerted [4+2] cycloaddition, forms an unstable endoperoxide. Subsequent ... has been investigated in both mechanistic and synthetic contexts. Rather than proceeding through a Type I or Type II ...
"An enzyme isolated from arteries transforms prostaglandin endoperoxides to an unstable substance that inhibits platelet ... Treprostinil is a synthetic analog of prostacyclin (PGI2). Treprostinil was approved for use in the United States in May 2002. ... This finding opened the door to a broader understanding of the role of prostaglandins in the body. Vane and a team from the ... During the 1960s a U.K. research team, headed by Professor John Vane began to explore the role of prostaglandins in anaphylaxis ...
Prostaglandins are signalled through two varying pathways cyclooxygenase (COX) (Also known as: prostaglandin-endoperoxide ... The drug is a synthetic androgen and anabolic steroid and hence is an agonist of the androgen receptor (AR), the biological ... ISBN 978-0-9828280-1-4. Zarkawi M, Galbraith H, Hutchinson JS (April 1991). "The action of trenbolone acetate, a synthetic ... Trenbolone acetate, or trenbolone 17β-acetate, is a synthetic estrane steroid and a derivative of nandrolone (19- ...
"An enzyme isolated from arteries transforms prostaglandin endoperoxides to an unstable substance that inhibits platelet ... Synthetic prostacyclin analogues (iloprost, cisaprost) are used intravenously, subcutaneously or by inhalation: as a ... Prostacyclin (also called prostaglandin I2 or PGI2) is a prostaglandin member of the eicosanoid family of lipid molecules. It ... prostaglandin I1, and prostaglandin I3". Journal of the American Chemical Society. 100 (24): 7690-7705. doi:10.1021/ja00492a043 ...
... enzymes to form prostaglandin endoperoxides. Specifically, prostaglandin G2 (PGG2) is modified by the peroxidase moiety of the ... The synthetic PGE2 dinoprostone has a plasma half-life of approximately 2.5-5 minutes, after vaginal administration, with most ... Prostaglandin E2 works as well as prostaglandin E1 in babies. Dinoprostone has important effects in labor by inducing softening ... Prostaglandin E2 (PGE2), along with other prostaglandins, are synthesized within the cortex and medulla of the kidney. The role ...
... also termed prostaglandin-endoperoxide synthase-1 (PTGS1) and PTGS2, respectively) metabolize arachidonic acid by adding ... A synthetic analog of RvE1 is in clinical phase III testing (see Phases of clinical research) for the treatment of the ... doi:10.1016/j.prostaglandins.2011.09.001. PMID 21945326. Matsuoka T, Narumiya S (2007). "Prostaglandin receptor signaling in ... Biosynthesis of prostaglandins); b) PGF synthase which converts PGH2 to PGF2α; c) Prostaglandin D2 synthase which converts PGH2 ...
Smith, W. L.; Song, I (2002). "The enzymology of prostaglandin endoperoxide H synthases-1 and -2". Prostaglandins & Other Lipid ... Note separate synthetic pathways, as described in section below.) Arachidonic acid is not one of the essential fatty acids. ... prostaglandin G/H synthase 1 and 2 {PTGS1 and PTGS2}) convert arachidonic acid to prostaglandin G2 and prostaglandin H2, which ... Arachidonic acid promotes the repair and growth of skeletal muscle tissue via conversion to prostaglandin PGF2alpha during and ...
Vezza R, Mezzasoma AM, Venditti G, Gresele P (2002). "Prostaglandin endoperoxides and thromboxane A2 activate the same receptor ... Several synthetic compounds bind to, but do not activate, TP and thereby inhibit its activation by activating ligands. These ... F2alpha-induced activation of its prostaglandin F receptor and prostaglandin E2-induced activation of its prostaglandin EP1 ... and prostaglandin D2-induced activation of its prostaglandin DP1 receptor cause TP receptor desensitization by activating ...

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