Adenosine: A nucleoside that is composed of ADENINE and D-RIBOSE. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter.Receptor, Adenosine A2A: A subclass of adenosine A2 receptors found in LEUKOCYTES, the SPLEEN, the THYMUS and a variety of other tissues. It is generally considered to be a receptor for ADENOSINE that couples to the GS, STIMULATORY G-PROTEIN.Receptor, Adenosine A1: A subtype of ADENOSINE RECEPTOR that is found expressed in a variety of tissues including the BRAIN and DORSAL HORN NEURONS. The receptor is generally considered to be coupled to the GI, INHIBITORY G-PROTEIN which causes down regulation of CYCLIC AMP.Adenosine Deaminase: An enzyme that catalyzes the hydrolysis of ADENOSINE to INOSINE with the elimination of AMMONIA.Receptor, Adenosine A3: A subtype of ADENOSINE RECEPTOR that is found expressed in a variety of locations including the BRAIN and endocrine tissues. The receptor is generally considered to be coupled to the GI, INHIBITORY G-PROTEIN which causes down regulation of CYCLIC AMP.Receptor, Adenosine A2B: A subclass of adenosine A2 receptors found in the CECUM, the COLON, the BLADDER, and a variety of other tissues. It is generally considered to be a low affinity receptor for ADENOSINE that couples to the GS, STIMULATORY G-PROTEIN.Adenosine Kinase: An enzyme that catalyzes the formation of ADP plus AMP from adenosine plus ATP. It can serve as a salvage mechanism for returning adenosine to nucleic acids. EC 2.7.1.20.Receptors, Adenosine A2: A subclass of ADENOSINE RECEPTORS that are generally considered to be coupled to the GS, STIMULATORY G-PROTEIN which causes up regulation of CYCLIC AMP.Adenosine A2 Receptor Agonists: Compounds that selectively bind to and activate ADENOSINE A2 RECEPTORS.Adenosine A2 Receptor Antagonists: Compounds that selectively bind to and block the activation of ADENOSINE A2 RECEPTORS.Receptors, Purinergic P1: A class of cell surface receptors that prefer ADENOSINE to other endogenous PURINES. Purinergic P1 receptors are widespread in the body including the cardiovascular, respiratory, immune, and nervous systems. There are at least two pharmacologically distinguishable types (A1 and A2, or Ri and Ra).Adenosine A1 Receptor Antagonists: Compounds that bind to and block the stimulation of ADENOSINE A1 RECEPTORS.Adenosine A1 Receptor Agonists: Compounds that bind to and stimulate ADENOSINE A1 RECEPTORS.Purinergic P1 Receptor Antagonists: Compounds that bind to and block the stimulation of PURINERGIC P1 RECEPTORS.Xanthines: Purine bases found in body tissues and fluids and in some plants.Purinergic P1 Receptor Agonists: Compounds that bind to and stimulate PURINERGIC P1 RECEPTORS.Adenosine Monophosphate: Adenine nucleotide containing one phosphate group esterified to the sugar moiety in the 2'-, 3'-, or 5'-position.Adenosine-5'-(N-ethylcarboxamide): A stable adenosine A1 and A2 receptor agonist. Experimentally, it inhibits cAMP and cGMP phosphodiesterase activity.Theophylline: A methyl xanthine derivative from tea with diuretic, smooth muscle relaxant, bronchial dilation, cardiac and central nervous system stimulant activities. Theophylline inhibits the 3',5'-CYCLIC NUCLEOTIDE PHOSPHODIESTERASE that degrades CYCLIC AMP thus potentiates the actions of agents that act through ADENYLYL CYCLASES and cyclic AMP.Adenosine A3 Receptor Antagonists: Compounds that selectively bind to and block the activation of ADENOSINE A3 RECEPTORS.Receptors, Purinergic: Cell surface proteins that bind PURINES with high affinity and trigger intracellular changes which influence the behavior of cells. The best characterized classes of purinergic receptors in mammals are the P1 receptors, which prefer ADENOSINE, and the P2 receptors, which prefer ATP or ADP.Adenosine A3 Receptor Agonists: Drugs that selectively bind to and activate ADENOSINE A3 RECEPTORS.2-Chloroadenosine: 2-Chloroadenosine. A metabolically stable analog of adenosine which acts as an adenosine receptor agonist. The compound has a potent effect on the peripheral and central nervous system.Phenethylamines: A group of compounds that are derivatives of beta- aminoethylbenzene which is structurally and pharmacologically related to amphetamine. (From Merck Index, 11th ed)Phenylisopropyladenosine: N-Isopropyl-N-phenyl-adenosine. Antilipemic agent. Synonym: TH 162.Inosine: A purine nucleoside that has hypoxanthine linked by the N9 nitrogen to the C1 carbon of ribose. It is an intermediate in the degradation of purines and purine nucleosides to uric acid and in pathways of purine salvage. It also occurs in the anticodon of certain transfer RNA molecules. (Dorland, 28th ed)5'-Nucleotidase: A glycoprotein enzyme present in various organs and in many cells. The enzyme catalyzes the hydrolysis of a 5'-ribonucleotide to a ribonucleoside and orthophosphate in the presence of water. It is cation-dependent and exists in a membrane-bound and soluble form. EC 3.1.3.5.Cyclic AMP: An adenine nucleotide containing one phosphate group which is esterified to both the 3'- and 5'-positions of the sugar moiety. It is a second messenger and a key intracellular regulator, functioning as a mediator of activity for a number of hormones, including epinephrine, glucagon, and ACTH.Adenosine Triphosphatases: A group of enzymes which catalyze the hydrolysis of ATP. The hydrolysis reaction is usually coupled with another function such as transporting Ca(2+) across a membrane. These enzymes may be dependent on Ca(2+), Mg(2+), anions, H+, or DNA.Tubercidin: An antibiotic purine ribonucleoside that readily substitutes for adenosine in the biological system, but its incorporation into DNA and RNA has an inhibitory effect on the metabolism of these nucleic acids.Adenine NucleotidesNucleoside Deaminases: Catalyze the hydrolysis of nucleosides with the elimination of ammonia.Coformycin: A ribonucleoside antibiotic synergist and adenosine deaminase inhibitor isolated from Nocardia interforma and Streptomyces kaniharaensis. It is proposed as an antineoplastic synergist and immunosuppressant.Dipyridamole: A phosphodiesterase inhibitor that blocks uptake and metabolism of adenosine by erythrocytes and vascular endothelial cells. Dipyridamole also potentiates the antiaggregating action of prostacyclin. (From AMA Drug Evaluations Annual, 1994, p752)Theobromine: 3,7-Dimethylxanthine. The principle alkaloid in Theobroma cacao (the cacao bean) and other plants. A xanthine alkaloid that is used as a bronchodilator and as a vasodilator. It has a weaker diuretic activity than THEOPHYLLINE and is also a less powerful stimulant of smooth muscle. It has practically no stimulant effect on the central nervous system. It was formerly used as a diuretic and in the treatment of angina pectoris and hypertension. (From Martindale, The Extra Pharmacopoeia, 30th ed, pp1318-9)Pentostatin: A potent inhibitor of ADENOSINE DEAMINASE. The drug induces APOPTOSIS of LYMPHOCYTES, and is used in the treatment of many lymphoproliferative malignancies, particularly HAIRY CELL LEUKEMIA. It is also synergistic with some other antineoplastic agents and has immunosuppressive activity.Adenosine Phosphosulfate: 5'-Adenylic acid, monoanhydride with sulfuric acid. The initial compound formed by the action of ATP sulfurylase on sulfate ions after sulfate uptake. Synonyms: adenosine sulfatophosphate; APS.Purines: A series of heterocyclic compounds that are variously substituted in nature and are known also as purine bases. They include ADENINE and GUANINE, constituents of nucleic acids, as well as many alkaloids such as CAFFEINE and THEOPHYLLINE. Uric acid is the metabolic end product of purine metabolism.Thioinosine: Sulfhydryl analog of INOSINE that inhibits nucleoside transport across erythrocyte plasma membranes, and has immunosuppressive properties. It has been used similarly to MERCAPTOPURINE in the treatment of leukemia. (From Martindale, The Extra Pharmacopoeia, 30th ed, p503)Triazines: Heterocyclic rings containing three nitrogen atoms, commonly in 1,2,4 or 1,3,5 or 2,4,6 formats. Some are used as HERBICIDES.Adenine: A purine base and a fundamental unit of ADENINE NUCLEOTIDES.Deoxyadenosines: Adenosine molecules which can be substituted in any position, but are lacking one hydroxyl group in the ribose part of the molecule.Purinergic Antagonists: Drugs that bind to and block the activation of PURINERGIC RECEPTORS.Kinetics: The rate dynamics in chemical or physical systems.Aminophylline: A drug combination that contains THEOPHYLLINE and ethylenediamine. It is more soluble in water than theophylline but has similar pharmacologic actions. It's most common use is in bronchial asthma, but it has been investigated for several other applications.Vasodilator Agents: Drugs used to cause dilation of the blood vessels.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Nucleoside Transport Proteins: Proteins involved in the transport of NUCLEOSIDES across cellular membranes.Hypoxanthine: A purine and a reaction intermediate in the metabolism of adenosine and in the formation of nucleic acids by the salvage pathway.Nucleotidases: A class of enzymes that catalyze the conversion of a nucleotide and water to a nucleoside and orthophosphate. EC 3.1.3.-.Hypoxanthines: Purine bases related to hypoxanthine, an intermediate product of uric acid synthesis and a breakdown product of adenine catabolism.TriazolesNucleosides: Purine or pyrimidine bases attached to a ribose or deoxyribose. (From King & Stansfield, A Dictionary of Genetics, 4th ed)Apyrase: A calcium-activated enzyme that catalyzes the hydrolysis of ATP to yield AMP and orthophosphate. It can also act on ADP and other nucleoside triphosphates and diphosphates. EC 3.6.1.5.Coronary Circulation: The circulation of blood through the CORONARY VESSELS of the HEART.Adenylate Cyclase: An enzyme of the lyase class that catalyzes the formation of CYCLIC AMP and pyrophosphate from ATP. EC 4.6.1.1.Bucladesine: A cyclic nucleotide derivative that mimics the action of endogenous CYCLIC AMP and is capable of permeating the cell membrane. It has vasodilator properties and is used as a cardiac stimulant. (From Merck Index, 11th ed)Cells, Cultured: Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.Guinea Pigs: A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.Ribonucleosides: Nucleosides in which the purine or pyrimidine base is combined with ribose. (Dorland, 28th ed)Rats, Sprague-Dawley: A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.Adenosylhomocysteinase: An enzyme which catalyzes the catabolism of S-ADENOSYLHOMOCYSTEINE to ADENOSINE and HOMOCYSTEINE. It may play a role in regulating the concentration of intracellular adenosylhomocysteine.Receptors, Purinergic P2: A class of cell surface receptors for PURINES that prefer ATP or ADP over ADENOSINE. P2 purinergic receptors are widespread in the periphery and in the central and peripheral nervous system.Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.Myocardium: The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.Rats, Wistar: A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.Nucleotides: The monomeric units from which DNA or RNA polymers are constructed. They consist of a purine or pyrimidine base, a pentose sugar, and a phosphate group. (From King & Stansfield, A Dictionary of Genetics, 4th ed)Dogs: The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)8-Bromo Cyclic Adenosine Monophosphate: A long-acting derivative of cyclic AMP. It is an activator of cyclic AMP-dependent protein kinase, but resistant to degradation by cyclic AMP phosphodiesterase.Colforsin: Potent activator of the adenylate cyclase system and the biosynthesis of cyclic AMP. From the plant COLEUS FORSKOHLII. Has antihypertensive, positive inotropic, platelet aggregation inhibitory, and smooth muscle relaxant activities; also lowers intraocular pressure and promotes release of hormones from the pituitary gland.Magnesium: A metallic element that has the atomic symbol Mg, atomic number 12, and atomic weight 24.31. It is important for the activity of many enzymes, especially those involved in OXIDATIVE PHOSPHORYLATION.Caffeine: A methylxanthine naturally occurring in some beverages and also used as a pharmacological agent. Caffeine's most notable pharmacological effect is as a central nervous system stimulant, increasing alertness and producing agitation. It also relaxes SMOOTH MUSCLE, stimulates CARDIAC MUSCLE, stimulates DIURESIS, and appears to be useful in the treatment of some types of headache. Several cellular actions of caffeine have been observed, but it is not entirely clear how each contributes to its pharmacological profile. Among the most important are inhibition of cyclic nucleotide PHOSPHODIESTERASES, antagonism of ADENOSINE RECEPTORS, and modulation of intracellular calcium handling.Extracellular Space: Interstitial space between cells, occupied by INTERSTITIAL FLUID as well as amorphous and fibrous substances. For organisms with a CELL WALL, the extracellular space includes everything outside of the CELL MEMBRANE including the PERIPLASM and the cell wall.Hyperemia: The presence of an increased amount of blood in a body part or an organ leading to congestion or engorgement of blood vessels. Hyperemia can be due to increase of blood flow into the area (active or arterial), or due to obstruction of outflow of blood from the area (passive or venous).1-Methyl-3-isobutylxanthine: A potent cyclic nucleotide phosphodiesterase inhibitor; due to this action, the compound increases cyclic AMP and cyclic GMP in tissue and thereby activates CYCLIC NUCLEOTIDE-REGULATED PROTEIN KINASESVasodilation: The physiological widening of BLOOD VESSELS by relaxing the underlying VASCULAR SMOOTH MUSCLE.Rabbits: The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.NorbornanesTime Factors: Elements of limited time intervals, contributing to particular results or situations.Perfusion: Treatment process involving the injection of fluid into an organ or tissue.Isoproterenol: Isopropyl analog of EPINEPHRINE; beta-sympathomimetic that acts on the heart, bronchi, skeletal muscle, alimentary tract, etc. It is used mainly as bronchodilator and heart stimulant.S-Adenosylhomocysteine: 5'-S-(3-Amino-3-carboxypropyl)-5'-thioadenosine. Formed from S-adenosylmethionine after transmethylation reactions.Purine Nucleosides: Purines with a RIBOSE attached that can be phosphorylated to PURINE NUCLEOTIDES.Radioligand Assay: Quantitative determination of receptor (binding) proteins in body fluids or tissue using radioactively labeled binding reagents (e.g., antibodies, intracellular receptors, plasma binders).Dinucleoside Phosphates: A group of compounds which consist of a nucleotide molecule to which an additional nucleoside is attached through the phosphate molecule(s). The nucleotide can contain any number of phosphates.Phosphodiesterase Inhibitors: Compounds which inhibit or antagonize the biosynthesis or actions of phosphodiesterases.RNA Editing: A process that changes the nucleotide sequence of mRNA from that of the DNA template encoding it. Some major classes of RNA editing are as follows: 1, the conversion of cytosine to uracil in mRNA; 2, the addition of variable number of guanines at pre-determined sites; and 3, the addition and deletion of uracils, templated by guide-RNAs (RNA, GUIDE).Equilibrative Nucleoside Transporter 1: A subtype of equilibrative nucleoside transporter proteins that is sensitive to inhibition by 4-nitrobenzylthioinosine.4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone: Inhibitor of phosphodiesterases.Adenosine Diphosphate Sugars: Esters formed between the aldehydic carbon of sugars and the terminal phosphate of adenosine diphosphate.Thionucleotides: Nucleotides in which the base moiety is substituted with one or more sulfur atoms.Purinergic P2 Receptor Antagonists: Compounds that bind to and block the stimulation of PURINERGIC P2 RECEPTORS.Guanosine: A purine nucleoside that has guanine linked by its N9 nitrogen to the C1 carbon of ribose. It is a component of ribonucleic acid and its nucleotides play important roles in metabolism. (From Dorland, 28th ed)Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.Rats, Inbred Strains: Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.Heart: The hollow, muscular organ that maintains the circulation of the blood.Signal Transduction: The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.Equilibrative-Nucleoside Transporter 2: A subtype of equilibrative nucleoside transporter proteins that is insensitive to inhibition by 4-nitrobenzylthioinosine.Platelet Aggregation: 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.Phosphotransferases: A rather large group of enzymes comprising not only those transferring phosphate but also diphosphate, nucleotidyl residues, and others. These have also been subdivided according to the acceptor group. (From Enzyme Nomenclature, 1992) EC 2.7.Enzyme Activation: Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.Glyburide: An antidiabetic sulfonylurea derivative with actions similar to those of chlorpropamide.Cell Membrane: The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.Suramin: A polyanionic compound with an unknown mechanism of action. It is used parenterally in the treatment of African trypanosomiasis and it has been used clinically with diethylcarbamazine to kill the adult Onchocerca. (From AMA Drug Evaluations Annual, 1992, p1643) It has also been shown to have potent antineoplastic properties.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Anoxia: Relatively complete absence of oxygen in one or more tissues.3',5'-Cyclic-AMP Phosphodiesterases: Enzymes that catalyze the hydrolysis of CYCLIC AMP to form adenosine 5'-phosphate. The enzymes are widely distributed in animal tissue and control the level of intracellular cyclic AMP. Many specific enzymes classified under this heading demonstrate additional spcificity for 3',5'-cyclic IMP and CYCLIC GMP.Formycins: Pyrazolopyrimidine ribonucleosides isolated from Nocardia interforma. They are antineoplastic antibiotics with cytostatic properties.Cyclic AMP-Dependent Protein Kinases: A group of enzymes that are dependent on CYCLIC AMP and catalyze the phosphorylation of SERINE or THREONINE residues on proteins. Included under this category are two cyclic-AMP-dependent protein kinase subtypes, each of which is defined by its subunit composition.Stimulation, Chemical: The increase in a measurable parameter of a PHYSIOLOGICAL PROCESS, including cellular, microbial, and plant; immunological, cardiovascular, respiratory, reproductive, urinary, digestive, neural, musculoskeletal, ocular, and skin physiological processes; or METABOLIC PROCESS, including enzymatic and other pharmacological processes, by a drug or other chemical.Purine-Nucleoside Phosphorylase: An enzyme that catalyzes the reaction between a purine nucleoside and orthophosphate to form a free purine plus ribose-5-phosphate. EC 2.4.2.1.Coronary Vessels: The veins and arteries of the HEART.AMP Deaminase: An enzyme that catalyzes the deamination of AMP to IMP. EC 3.5.4.6.Potassium Channels: Cell membrane glycoproteins that are selectively permeable to potassium ions. At least eight major groups of K channels exist and they are made up of dozens of different subunits.Cattle: Domesticated bovine animals of the genus Bos, usually kept on a farm or ranch and used for the production of meat or dairy products or for heavy labor.Purinergic P2 Receptor Agonists: Compounds that bind to and stimulate PURINERGIC P2 RECEPTORS.Ischemic Preconditioning, Myocardial: Exposure of myocardial tissue to brief, repeated periods of vascular occlusion in order to render the myocardium resistant to the deleterious effects of ISCHEMIA or REPERFUSION. The period of pre-exposure and the number of times the tissue is exposed to ischemia and reperfusion vary, the average being 3 to 5 minutes.Potassium: An element in the alkali group of metals with an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte that plays a significant role in the regulation of fluid volume and maintenance of the WATER-ELECTROLYTE BALANCE.Ribose: A pentose active in biological systems usually in its D-form.Binding Sites: The parts of a macromolecule that directly participate in its specific combination with another molecule.Dilazep: Coronary vasodilator with some antiarrhythmic activity.Hydrogen-Ion Concentration: The normality of a solution with respect to HYDROGEN ions; H+. It is related to acidity measurements in most cases by pH = log 1/2[1/(H+)], where (H+) is the hydrogen ion concentration in gram equivalents per liter of solution. (McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)Uridine Triphosphate: Uridine 5'-(tetrahydrogen triphosphate). A uracil nucleotide containing three phosphate groups esterified to the sugar moiety.Affinity Labels: Analogs of those substrates or compounds which bind naturally at the active sites of proteins, enzymes, antibodies, steroids, or physiological receptors. These analogs form a stable covalent bond at the binding site, thereby acting as inhibitors of the proteins or steroids.Mice, Inbred C57BLDideoxyadenosine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is an inhibitor of HIV replication, acting as a chain-terminator of viral DNA by binding to reverse transcriptase. Its principal side effect is nephrotoxicity. In vivo, dideoxyadenosine is rapidly metabolized to DIDANOSINE (ddI) by enzymatic deamination; ddI is then converted to dideoxyinosine monophosphate and ultimately to dideoxyadenosine triphosphate, the putative active metabolite.Isopentenyladenosine: N(6)-[delta(3)-isopentenyl]adenosine. Isopentenyl derivative of adenosine which is a member of the cytokinin family of plant growth regulators.Depression, Chemical: The decrease in a measurable parameter of a PHYSIOLOGICAL PROCESS, including cellular, microbial, and plant; immunological, cardiovascular, respiratory, reproductive, urinary, digestive, neural, musculoskeletal, ocular, and skin physiological processes; or METABOLIC PROCESS, including enzymatic and other pharmacological processes, by a drug or other chemical.

Analysis of a ubiquitous promoter element in a primitive eukaryote: early evolution of the initiator element. (1/6258)

Typical metazoan core promoter elements, such as TATA boxes and Inr motifs, have yet to be identified in early-evolving eukaryotes, underscoring the extensive divergence of these organisms. Towards the identification of core promoters in protists, we have studied transcription of protein-encoding genes in one of the earliest-diverging lineages of Eukaryota, that represented by the parasitic protist Trichomonas vaginalis. A highly conserved element, comprised of a motif similar to a metazoan initiator (Inr) element, surrounds the start site of transcription in all examined T. vaginalis genes. In contrast, a metazoan-like TATA element appears to be absent in trichomonad promoters. We demonstrate that the conserved motif found in T. vaginalis protein-encoding genes is an Inr promoter element. This trichomonad Inr is essential for transcription, responsible for accurate start site selection, and interchangeable between genes, demonstrating its role as a core promoter element. The sequence requirements of the trichomonad Inr are similar to metazoan Inrs and can be replaced by a mammalian Inr. These studies show that the Inr is a ubiquitous, core promoter element for protein-encoding genes in an early-evolving eukaryote. Functional and structural similarities between this protist Inr and the metazoan Inr strongly indicate that the Inr promoter element evolved early in eukaryotic evolution.  (+info)

Expression of both P1 and P2 purine receptor genes by human articular chondrocytes and profile of ligand-mediated prostaglandin E2 release. (2/6258)

OBJECTIVE: To assess the expression and function of purine receptors in articular chondrocytes. METHODS: Reverse transcriptase-polymerase chain reaction (RT-PCR) was used to screen human chondrocyte RNA for expression of P1 and P2 purine receptor subtypes. Purine-stimulated prostaglandin E2 (PGE2) release from chondrocytes, untreated or treated with recombinant human interleukin-1alpha (rHuIL-1alpha), was assessed by radioimmunoassay. RESULTS: RT-PCR demonstrated that human articular chondrocytes transcribe messenger RNA for the P1 receptor subtypes A2a and A2b and the P2 receptor subtype P2Y2, but not for the P1 receptor subtypes A1 and A3. The P1 receptor agonists adenosine and 5'-N-ethylcarboxamidoadenosine did not change PGE2 release from chondrocytes. The P2Y2 agonists ATP and UTP stimulated a small release of PGE2 that was potentiated after pretreatment with rHuIL-1alpha. PGE2 release in response to ATP and UTP cotreatment was not additive, but release in response to coaddition of ATP and bradykinin (BK) or UTP and BK was additive, consistent with ATP and UTP competition for the same receptor site. The potentiation of PGE2 release in response to ATP and UTP after rHuIL-1alpha pretreatment was mimicked by phorbol myristate acetate. CONCLUSION: Human chondrocytes express both P1 and P2 purine receptor subtypes. The function of the P1 receptor subtype is not yet known, but stimulation of the P2Y2 receptor increases IL-1-mediated PGE2 release.  (+info)

Presynaptic action of adenosine on a 4-aminopyridine-sensitive current in the rat carotid body. (3/6258)

1. Plasma adenosine concentration increases during hypoxia to a level that excites carotid body chemoreceptors by an undetermined mechanism. We have examined this further by determining the electrophysiological responses to exogenous adenosine of sinus nerve chemoafferents in vitro and of whole-cell currents in isolated type I cells. 2. Steady-state, single-fibre chemoafferent discharge was increased approximately 5-fold above basal levels by 100 microM adenosine. This adenosine-stimulated discharge was reversibly and increasingly reduced by methoxyverapamil (D600, 100 microM), by application of nickel chloride (Ni2+, 2 mM) and by removal of extracellular Ca2+. These effects strongly suggest a presynaptic, excitatory action of adenosine on type I cells of the carotid body. 3. Adenosine decreased whole-cell outward currents at membrane potentials above -40 mV in isolated type I cells recorded during superfusion with bicarbonate-buffered saline solution at 34-36 C. This effect was reversible and concentration dependent with a maximal effect at 10 microM. 4. The degree of current inhibition induced by 10 microM adenosine was voltage independent (45.39 +/- 2. 55 % (mean +/- s.e.m.) between -40 and +30 mV) and largely ( approximately 75 %), but not entirely, Ca2+ independent. 4-Aminopyridine (4-AP, 5 mM) decreased the amplitude of the control outward current by 80.60 +/- 3.67 % and abolished the effect of adenosine. 5. Adenosine was without effect upon currents near the resting membrane potential of approximately -55 mV and did not induce depolarization in current-clamp experiments. 6. We conclude that adenosine acts to inhibit a 4-AP-sensitive current in isolated type I cells of the rat carotid body and suggest that this mechanism contributes to the chemoexcitatory effect of adenosine in the whole carotid body.  (+info)

A comparison of an A1 adenosine receptor agonist (CVT-510) with diltiazem for slowing of AV nodal conduction in guinea-pig. (4/6258)

1. The purpose of this study was to compare the pharmacological properties (i.e. the AV nodal depressant, vasodilator, and inotropic effects) of two AV nodal blocking agents belonging to different drug classes; a novel A1 adenosine receptor (A1 receptor) agonist, N-(3(R)-tetrahydrofuranyl)-6-aminopurine riboside (CVT-510), and the prototypical calcium channel blocker diltiazem. 2. In the atrial-paced isolated heart, CVT-510 was approximately 5 fold more potent to prolong the stimulus-to-His bundle (S-H interval), a measure of slowing AV nodal conduction (EC50 = 41 nM) than to increase coronary conductance (EC50 = 200 nM). At concentrations of CVT-510 (40 nM) and diltiazem (1 microM) that caused equal prolongation of S-H interval (approximately 10 ms), diltiazem, but not CVT-510, significantly reduced left ventricular developed pressure (LVP) and markedly increased coronary conductance. CVT-510 shortened atrial (EC50 = 73 nM) but not the ventricular monophasic action potentials (MAP). 3. In atrial-paced anaesthetized guinea-pigs, intravenous infusions of CVT-510 and diltiazem caused nearly equal prolongations of P-R interval. However, diltiazem, but not CVT-510, significantly reduced mean arterial blood pressure. 4. Both CVT-510 and diltiazem prolonged S-H interval, i.e., slowed AV nodal conduction. However, the A1 receptor-selective agonist CVT-510 did so without causing the negative inotropic, vasodilator, and hypotensive effects associated with diltiazem. Because CVT-510 did not affect the ventricular action potential, it is unlikely that this agonist will have a proarrythmic action in ventricular myocardium.  (+info)

A new synthesis of 5'-deoxy-8,5'-cyclo-adenosine and -inosine: conformationally-fixed purine nucleosides (nucleosides and nucleotides. XVI). (5/6258)

A versatile method for the synthesis of 5'-deoxy-8,5'-cycloadenosine, a conformationally-fixed "anti" type of adenosine, was presented. Irradiation of 2', 3'-O-isopropylidene-5'-deoxy-5'-phenylthioadenosine with 60W Hg vapor lamp afforded 2',3'-O-isopropylidene-5'-deoxy-8,5'-cycloadenosine in high yield. The use of other 5'-alkylthio derivatives also gave the cycloadenosine, though the yields were rather poor. Deacetonation of the cyclocompound with 0.1N HCl gave 5'-deoxy-8,5'-cycloadenosine. The cycloinosine derivative was similarly prepared. The nmr, mass and CD spectra of 5'-deoxy-8,5'-cycloadenosine were given and discussed with the previously reported results.  (+info)

End group of naturally terminated and UV lesion terminated T7 in vitro RNA. (6/6258)

The 3' terminal nucleosides of RNA transcribed in vitro by E. coli RNA polymerase from T7 DNA and UV irradiated TN DNA were determined. The 3' terminal nucleoside of naturally terminated (t1 termination site) RNA cytidine. In the case of RNA terminated at UV lesions, it is cytidine in 0 per cent of the molecules and adenosine in the remaining 30 per cent. Cytidine trialcohols are labile in high concentrations of KOH and at high temperature and appear to convert to uridine.  (+info)

Nucleoside-3'-phosphotriesters as key intermediates for the oligoribonucleotide synthesis. III. An improved preparation of nucleoside 3'-phosphotriesters, their 1H NMR characterization and new conditions for removal of 2-cyanoethyl group. (7/6258)

An improved procedure for the transformation of 5'-O-monomethoxytrityl-2'-O-acetyl-3'-phosphates of uridine la, inosine ib and 6-N-benzoyladenosine lc into corresponding 3'/2,2,2-trichloroethyl, 2-cyanoethyl/-phosphates iiaic is reported. H NMR characterization of nucleoside 3'-phosphotriesters is presented. New conditions i.e. anhydrous triethylamine-pyridine treatment have been found for the selective removal of 2-cyanoethyl group from nucleoside 3'-phosphotriesters in the presence of neighbouring 2'-O-acetyl one.  (+info)

Electrophysiologic effects of adenosine in patients with supraventricular tachycardia. (8/6258)

BACKGROUND: We correlated the electrophysiologic (EP) effects of adenosine with tachycardia mechanisms in patients with supraventricular tachycardias (SVT). METHODS AND RESULTS: Adenosine was administered to 229 patients with SVTs during EP study: atrioventricular (AV) reentry (AVRT; n=59), typical atrioventricular node reentry (AVNRT; n=82), atypical AVNRT (n=13), permanent junctional reciprocating tachycardia (PJRT; n=12), atrial tachycardia (AT; n=53), and inappropriate sinus tachycardia (IST; n=10). There was no difference in incidence of tachycardia termination at the AV node in AVRT (85%) versus AVNRT (86%) after adenosine, but patients with AVRT showed increases in the ventriculoatrial (VA) intervals (13%) compared with typical AVNRT (0%), P<0.005. Changes in atrial, AV, or VA intervals after adenosine did not predict the mode of termination of long R-P tachycardias. For patients with AT, there was no correlation with location of the atrial focus and adenosine response. AV block after adenosine was only observed in AT patients (27%) or IST (30%). Patients with IST showed atrial cycle length increases after adenosine (P<0.05) with little change in activation sequence. The incidence of atrial fibrillation after adenosine was higher for those with AVRT (15%) compared with typical AVNRT (0%) P<0.001, or atypical AVNRT (0%) but similar to those with AT (11%) and PJRT (17%). CONCLUSIONS: The EP response to adenosine proved of limited value to identify the location of AT or SVT mechanisms. Features favoring AT were the presence of AV block or marked shortening of atrial cycle length before tachycardia suppression. Atrial fibrillation was more common after adenosine in patients with AVRT, PJRT, or AT. Patients with IST showed increases in cycle length with little change in atrial activation sequence after adenosine.  (+info)

TY - JOUR. T1 - Chronic exposure to adenosine receptor agonists and antagonists reciprocally regulates the A1 adenosine receptor-adenylyl cyclase system in cerebellar granule cells. AU - Hettinger-Smith, Barbara D.. AU - Leid, Mark. AU - Murray, Thomas F.. PY - 1996/11. Y1 - 1996/11. N2 - Chronic treatment with the adenosine receptor antagonist caffeine evokes an up-regulation of A1 adenosine receptors and increased coupling of the receptor to G proteins in rat brain membranes. However, chronic agonist exposure has not been explored. Primary cultures of cerebellar granule cells were exposed chronically to A1 adenosine receptor agonists and antagonists. Exposure to the A1 adenosine receptor agonist N6-cyclopentyladenosine resulted in (1) a time- and concentration-dependent reduction in the density of receptors labeled by 1,3[3H]dipropyl-8-cyclopentylxanthine, (2) an enhanced ability of guanyl nucleotides to decrease the fraction of A1 adenosine receptor sites displaying high affinity for ...
Intravenously administered adenosine is rapidly cleared from the circulation via cellular uptake, primarily by erythrocytes and vascular endothelial cells. This process involves a specific transmembrane nucleoside carrier system that is reversible, nonconcentrative, and bidirectionally symmetrical. Intracellular adenosine is rapidly metabolized either via phosphorylation to adenosine monophosphate by adenosine kinase, or via deamination to inosine by adenosine deaminase in the cytosol. Since adenosine kinase has a lower Km and Vmax than adenosine deaminase, deamination plays a significant role only when cytosolic adenosine saturates the phosphorylation pathway. Inosine formed by deamination of adenosine can leave the cell intact or can be degraded to hypoxanthine, xanthine, and ultimately uric acid. Adenosine monophosphate formed by phosphorylation of adenosine is incorporated into the high-energy phosphate pool. While extracellular adenosine is primarily cleared by cellular uptake with a ...
Adenosine is a candidate sleep substance. It can be both a distress signal of importance in pathology and a physiological regulator. Key factors in determining which of these possibilities pertain are: (i) the number of receptors expressed, and (ii) the mechanisms that establish extracellular adenosine levels. The roles of adenosine are studied by means of antagonists and/or animals (mostly mice) with targeted deletions of receptors or enzymes involved in adenosine metabolism. Whereas adaptive changes in the genetically modified mice can occur for the physiologically important effects, such adaptive changes are less likely to occur in situations where adenosine acts as a distress signal. The relevance to sleep will be covered only in general terms in this review and will be covered in other contributions to this volume.
Adenosine is a nucleoside that is composed of adenine and d-ribose. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. For instance, adenosine plays an important role in energy transfer - as adenosine triphosphate (ATP) and adenosine diphosphate (ADP). It also plays a role in signal transduction as cyclic adenosine monophosphate, cAMP. Adenosine itself is both a neurotransmitter and potent vasodilator. When administered intravenously, adenosine causes transient heart block in the AV node. Because of the effects of adenosine on AV node-dependent supraventricular tachycardia, adenosine is considered a class V antiarrhythmic agent ...
Having the ability to modulate lymphocyte entry into the central nervous system (CNS) would benefit patients with neuroinflammatory diseases. We have previously shown that extracellular adenosine regulates CNS entry of lymphocytes during experimental autoimmune encephalomyelitis (EAE), the animal model for the CNS inflammatory disease multiple sclerosis. For instance, while extracellular adenosine levels are vastly increased following inflammatory cellular damage (from the hydrolysis of released cytoplasimic ATP by CD39 and CD73), mice lacking CD73 or given adenosine receptor (AR) antagonists have significantly reduced CNS lymphocyte entry during EAE. We now show through detailed genetic studies that AR signaling regulates lymphocyte migration into the CNS though induction of CX3CL1, a specialized chemokine that acts as both an adhesion molecule and chemoattractant for lymphocytes, monocytes, and NK cells. We show that AR signaling is necessary and sufficient to induce CNS expression of CX3CL1 ...
Vasodilator stress with adenosine or dipyridamole is an alternative to exercise stress with myocardial perfusion imaging for the detection of coronary artery disease. Although the safety of adenosine and dipyridamole has been well established, undesirable side effects including chest pain, headache, dyspnea, and atrioventricular conduction abnormalities do occur in a majority of patients.1-4 In addition, both adenosine and dipyridamole produce severe bronchoconstriction when given to asthmatics. Because of its ultrashort half-life, adenosine must be administered by a constant IV infusion.. Whereas adenosine-induced coronary vasodilatation is mediated primarily by stimulation of the A2A receptor subtype on vascular smooth muscle, the side effects described above are believed to be caused by stimulation of 1 or more of the other 3 adenosine receptor subtypes, A1, A2B, and A3.5 The discovery of highly selective and relatively short-acting adenosine receptor A2A agonists6-9 has opened the ...
A concise synthesis of a series of N6-substituted adenosines with bicyclo[3.2.1]octan-6-yl and polycyclic N6-substituents has been developed. The adenosine A1 receptor (A1R) affinity and potency of these compounds was initially assessed using competitive binding assays and cyclic adenosine monophosphate (cAMP) accumulation assays in DDT1 MF-2 cells. The potency and receptor subtype selectivity of selected examples was further evaluated by measuring their effects on cAMP accumulation at all human adenosine receptor subtypes expressed in CHO cells. The results of these assays indicated that all of the synthesised N6-substituted adenosines are full agonists at A1R and activate this receptor selectively over the other adenosine receptor subtypes. The two standout compounds in terms of potency were N6-(3-thiabicyclo[3.2.1]octan-6-yl)adenosine and N6-(cubanylmethyl)adenosine with EC50 values at human A1R of 2.3 nM and 1.1 nM, respectively. The cubanylmethyl derivative in particular proved to be highly ...
We examined how the endogenous anticonvulsant adenosine might influence gamma-aminobutyric acid type A (GABA(A)) receptor stability and which adenosine receptors (ARs) were involved. Upon repetitive activation (GABA 500 microM), GABA(A) receptors, microtransplanted into Xenopus oocytes from neurosurgically resected epileptic human nervous tissues, exhibited an obvious GABA(A)-current (I(GABA)) run-down, which was consistently and significantly reduced by treatment with the nonselective adenosine receptor antagonist CGS15943 (100 nM) or with adenosine deaminase (ADA) (1 units/ml), that inactivates adenosine. It was also found that selective antagonists of A2B (MRS1706, 10 nM) or A3 (MRS1334, 30 nM) receptors reduced I(GABA) run-down, whereas treatment with the specific A1 receptor antagonist DPCPX (10 nM) was ineffective. The selective A2A receptor antagonist SCH58261 (10 nM) reduced or potentiated I(GABA) run-down in approximately 40% and approximately 20% of tested oocytes, respectively. The ...
Introduction: Prior studies demonstrate that ischemic preconditioning (IP) alters adenosine metabolism. The significance of this effect is not fully understood, but evidence suggests that reduction in extracellular adenosine may represent use as an alternative fuel. Transformation into AMP/ADP may also replenish intracellular total adenine nucleotides (TAN), improving the potential high-energy phosphate bonds available in cells facing ischemia. In both cases, adenosine supports cell energy requirements and may be a key component of IPs protective mechanisms. There are no previous studies of brain adenosine in human patients undergoing remote IP.. Methods: In adults with aneurysmal subarachnoid hemorrhage (SAH), 3-4 remote IP sessions were conducted on non-consecutive days, 4-12 days after hemorrhage. Each session consisted of 4 5-min cycles of lower extremity blood pressure cuff inflation to 30mmHg above systolic blood pressure, followed by 5-min reperfusion. Patients had microdialysis (MD) ...
To the Editor: Recently, Jeremias et al1 reported their studies comparing the vasodilator action of intracoronary injected adenosine with ATP in 6 healthy mongrel dogs. On the basis of a dose-response curve ranging from 10 to 100 μg, the authors conclude that adenosine and ATP are approximately equipotent vasodilators. Neither substance could induce maximal vasodilation, as assessed with postischemic hyperemia. Similar results were obtained by Kato et al2 in the human coronary vasculature using a single dose of adenosine and ATP (20 μg), without comparison with postischemic hyperemia. Both groups conclude that adenosine and ATP are equipotent coronary vasodilators and suggest that the ATP-induced vasodilation is caused by its degradation to AMP and adenosine, with subsequent stimulation of adenosine A2 receptors. We disagree their conclusions for the following 2 reasons:. 1. Equimolar doses of ATP and adenosine should be compared. The molecular weight of ATP is roughly twice that of adenosine ...
Intra- and extracellular adenosine levels rise in response to physiological stimuli and with metabolic/energetic perturbations, inflammatory challenge and tissue injury. Extracellular adenosine engages members of the G-protein coupled adenosine receptor (AR) family to mediate generally beneficial acute and adaptive responses within all constituent cells of the heart. In this way the four AR sub-types - A1, A2A, A2B, and A 3Rs - regulate myocardial contraction, heart rate and conduction, adrenergic control, coronary vascular tone, cardiac and vascular growth, inflammatory-vascular cell interactions, and cellular stress-resistance, injury and death. The AR sub-types exert both distinct and overlapping effects, and may interact in mediating these cardiovascular responses. The roles of the ARs in beneficial modulation of cardiac and vascular function, growth and stress-resistance render them attractive therapeutic targets. However, interactions between ARs and with other receptors, and their ubiquitous
Adenosine is an important mediator of the endogenous defense against ischemia-induced injury in the heart. Adenosine can achieve cardioprotection by mediating the effect of ischemic preconditioning and by protecting against myocyte injury when it is present during the infarct-producing ischemia. A novel adenosine A3 receptor can mediate this protective function. One approach to achieve cardioprotection is to enhance myocardial sensitivity to the endogenous adenosine by increasing the number of adenosine receptors instead of administering an adenosine receptor agonist. The objective of the present study was to investigate whether genetic manipulation of the cardiac myocyte, achieved by gene transfer and overexpression of the human A3 receptor cDNA, renders the myocytes resistant to the deleterious effect of ischemia. Prolonged hypoxia with glucose deprivation, causing myocyte injury and adenosine release, was used to simulate ischemia in cultured chick embryo ventricular myocytes. During simulated
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We have demonstrated previously that both acute and chronic oral administration of adenosine have novel functions such as anti-hypertensive effects and improved hyperlipidaemia in stroke-prone spontaneously hypertensive rats (SHRSP) fed a normal diet. The purpose of the present study was to investigate the effect of adenosine administration on metabolic syndrome-related parameters in SHRSP fed a high-fat diet. Six-week-old rats were divided into three groups, and were administered either water (control) or adenosine (10 or 100 mg/l) for 8 weeks. During this period, the rats had free access to a high-fat diet based on AIN-93M. The results showed that hypertension, plasma lipid, NO, insulin, glucose and urinary 8-hydroxy-2-deoxyguanosine levels improved significantly in both adenosine groups. The mRNA expression levels of genes involved in anti-oxidative activity and adenosine receptors were also altered in the adenosine groups. Administration of adenosine also increased plasma adiponectin ...
Cyclic 3, 5-[14C]AMP was measured in platelets that had first been incubated with [14C]adenine. Maximum increases of 2-4-fold were observed 0.5 min after addition of 10-40 µM adenosine. Smaller increases were obtained with higher concentrations of adenosine. In 0.5-min incubations 2-chloroadenosine was less effective than adenosine at concentrations below 20 µM and more effective at concentrations above 100 µM. Incorporation of 1-10 µM adenosine into platelets was inhibited at least 96% by p-nitrobenzylthioguanosine without any effect on the increase in cyclic [14C]AMP caused by these concentrations of adenosine, suggesting that adenosine acts at an extracellular site. With higher adenosine concentrations, p-nitrobenzylthioguanosine was less effective in inhibiting incorporation of adenosine but blocked the decline in cyclic [14C]AMP levels observed on increasing the adenosine concentration above 40 µM. This inhibitory effect of high adenosine concentrations on the accumulation of cyclic ...
Each type of adenosine receptor has different functions, although with some overlap.[3] For instance, both A1 receptors and A2A play roles in the heart, regulating myocardial oxygen consumption and coronary blood flow, while the A2A receptor also has broader anti-inflammatory effects throughout the body.[4] These two receptors also have important roles in the brain,[5] regulating the release of other neurotransmitters such as dopamine and glutamate,[6][7][8] while the A2B and A3 receptors are located mainly peripherally and are involved in processes such as inflammation and immune responses. Most older compounds acting on adenosine receptors are nonselective, with the endogenous agonist adenosine being used in hospitals as treatment for severe tachycardia (rapid heart beat),[9] and acting directly to slow the heart through action on all four adenosine receptors in heart tissue,[10] as well as producing a sedative effect through action on A1 and A2A receptors in the brain. Xanthine derivatives ...
Regadenoson produced higher stress MBF than dipyridamole and adenosine (3.58 ± 0.58 vs. 2.81 ± 0.67 vs. 2.78 ± 0.61 ml/min/g, p = 0.0009 and p = 0.0008 respectively). Regadenoson had a much higher heart rate response than adenosine and dipyridamole respectively (95 ± 11 vs. 76 ± 13 vs. 86 ± 12 beats/ minute) When stress MBF was adjusted for heart rate, there were no differences between regadenoson and adenosine (37.8 ± 6 vs. 36.6 ± 4 μl/sec/g, p = NS), but differences between regadenoson and dipyridamole persisted (37.8 ± 6 vs. 32.6 ± 5 μl/sec/g, p = 0.03). The unadjusted MPR was higher with regadenoson (3.11 ± 0.63) when compared with adenosine (2.7 ± 0.61, p = 0.02) and when compared with dipyridamole (2.61 ± 0.57, p = 0.04). Similar to stress MBF, these differences in MPR between regadenoson and adenosine were abolished when adjusted for heart rate (2.04 ± 0.34 vs. 2.12 ± 0.27, p = NS), but persisted between regadenoson and dipyridamole (2.04 ± 0.34 vs. 1.77 ± 0.33, p = ...
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In the central nervous system, the nucleoside adenosine regulates neuronal activity by modulating the actions of other neurotransmitter systems, thereby influencing many different physiological processes and behaviors. Adenosinergic mechanisms are especially important in fine-tuning glutamatergic neurotransmission. Astrocytic release of adenosine triphosphate and its subsequent extracellular breakdown provides adenosine to drive homeostatic sleep. Acute ethanol (alcohol) exposure increases extracellular adenosine, which mediates the ataxic and hypnotic/sedative effects of alcohol, while chronic ethanol exposure leads to downregulated adenosine signaling that underlies insomnia, a major predictor of relapse. Adenosine gates glutamatergic input to the circadian clock located in the suprachiasmatic nucleus of the hypothalamus, modulating both photic (light-induced) and nonphotic (behaviorally-induced) synchronization of circadian activity rhythms. A recent study using mice lacking the equilibrative ...
Adenosine mediates many physiological functions via activation of extracellular receptors. The modulation of cell growth by adenosine was found to be receptor-mediated. In A431 cells adenosine evoked a biphasic response in which a low concentration (~10 μM) produced inhibition of colony formation but at higher concentrations (up to 100 μM) this inhibition was progressively reversed. Evidence for the involvement of A1 (inhibitory) and A2 (stimulatory) adenosine receptors in regulating cell growth of these tumor cells was obtained through plating efficiency studies based on the relative potency of adenosine agonists and antagonists. When both A1 and A2 receptors were blocked, colony formation or growth was not inhibited at low concentrations of adenosine but was inhibited at high adenosine concentrations ...
The initial studies to test the hypothesis that adenosine release mediates the anti-inflammatory effects of methotrexate were performed in vitro. In these studies, methotrexate treatment increased adenosine release from cultured endothelial cells and fibroblasts and the adenosine released diminished stimulated neutrophil adhesion to the monolayers of cultured cells (Cronstein et al., 1991). Subsequent in vivo studies confirmed the hypothesis that adenosine mediates the anti-inflammatory effects of methotrexate; pharmacologically relevant doses of methotrexate induce intracellular AICAR accumulation in splenocytes, increase adenosine concentrations in inflammatory exudates, and diminish leukocyte accumulation at an inflamed site (Cronstein et al., 1993). Moreover, the increase in exudate adenosine concentration was responsible for the anti-inflammatory effects of the drug since adenosine receptor antagonists or adenosine deaminase, an enzyme which converts adenosine to the receptor-inactive ...
Our work demonstrates that human endothelial cells of disparate origin are characterized by differential expression of adenosine receptor subtypes. HUVECs express mRNA for A2A and A2B receptors at a ratio of 10:1, and this preferential gene expression agrees well with the typical pharmacological phenotype of A2A receptor-mediated simulation of adenylate cyclase by adenosine analogs. Using complementary techniques, RT-PCR, and gene expression array, we found that A1 and A3 adenosine receptors are not expressed in HUVECs. Previous studies in HUVECs have suggested a potential role of A1 receptor in maintaining endothelial barrier function4 and of A1 and A3 receptors in modulation of tissue factors expression.6 The apparent contradiction between these results and ours can be explained by the use of nonselective concentrations of adenosine receptor ligands in previous studies.. HMEC-1 also express only A2A and A2B mRNA, but in contrast to HUVECs, they express predominantly A2B receptor mRNA, with a ...
Adenosine receptors (AR) belong to the G-protein coupled receptor family. There are four receptor subtypes: A1, A2A, A2B e A3. Adenosine receptor subtypes show a different distribution in the organism and are implicated in several physiopathological processes. In particular, antagonists towards A1AR are promising in the treatment of cognitive disorders. A2A antagonists seem to be involved in decrease the neurological impairment observed in Parkinson’s disease. A2B antagonists are potential therapeutic agents in asthma and diabetes. Finally, antagonists at the A3AR could be implicated in tumor growth inhibition and in glaucoma treatment. The crystallographic structure acquisition of the human A2A receptor allowed the design of new AR antagonists by the help of computational techniques. Our group is focused on the synthesis of new adenosine receptor antagonists (particularly towards A2A and A3) for their potential therapeutic use, but also as tools for pharmacological investigations on ...
Summary 1. The effect of the adenosine A2 receptor (AdoA2R) agonist N6-[2-(3,5-dimethoxyphenyl)-2-(2-methylphenyl)-ethyl]adenosine (DPMA) on adenosine A1 receptor (AdoA1R)-mediated negative inotropic responses was investigated in rat heart. 2. Hearts from male Wistar rats (250-350 g) were perfused with Krebs-Henseleit solution at constant flow in non-recirculating Langendorff mode. Hearts were paced at 5 Hz (5 ms duration, supramaximal voltage) via ventricular electrodes. After 30 min equilibration, (R)-N6-phenylisopropyl adenosine (R-PIA) concentration-response curves were constructed in the absence or presence of DPMA. 3. In paced hearts, R-PIA induced concentration-dependent decreases in triple product (heart rate נpeak systolic developed pressure נdP?/?dtmax), which were significantly attenuated by 1 nmol?/?L DPMA with a shift in pEC50 from 8.0 ᠰ.5 (n = 9) in control hearts to 6.63 ᠱ.03 (n = 5) in treated tissues (P , 0.05). The AdoA2AR antagonist 8-(3-chlorostyryl)caffeine (1 ...
P>Adenosine is a well-described anti-inflammatory modulator of immune responses within peripheral tissues. Extracellular adenosine accumulates in inflamed and damaged tissues and inhibits the effector functions of various immune cell populations, including CD8 T cells. However, it remains unclear whether extracellular adenosine also regulates the initial activation of naive CD8 T cells by professional and semi-professional antigen-presenting cells, which determines their differentiation into effector or tolerant CD8 T cells, respectively. We show that adenosine inhibited the initial activation of murine naive CD8 T cells after alpha CD3/CD28-mediated stimulation. Adenosine caused inhibition of activation, cytokine production, metabolic activity, proliferation and ultimately effector differentiation of naive CD8 T cells. Remarkably, adenosine interfered efficiently with CD8 T-cell priming by professional antigen-presenting cells (dendritic cells) and semi-professional antigen-presenting cells ...
The review summarizes data evaluating the role of adenosine receptor signaling in murine hematopoietic functions. The studies carried out utilized either non-selective activation of adenosine receptors induced by elevation of extracellular adenosine or by administration of synthetic adenosine analogs having various proportions of selectivity for a particular receptor. Numerous studies have described stimulatory effects of non-selective activation of adenosine receptors, manifested as enhancement of proliferation of cells at various levels of the hematopoietic hierarchy. Subsequent experimental approaches, considering the hematopoiesis-modulating action of adenosine receptor agonists with a high level of selectivity to individual adenosine receptor subtypes, have revealed differential effects of various adenosine analogs. Whereas selective activation of A(1) receptors has resulted in suppression of proliferation of hematopoietic progenitor and precursor cells, that of A(3) receptors has led to ...
Recent evidence suggests that ethanol initially causes an increase in receptor-dependent cAMP levels, followed by heterologous desensitization of receptors coupled to GS after chronic exposure. Here we investigated the role of adenosine in mediating these responses. We found that ethanol caused accumulation of extracellular adenosine in NG108-15 and S49 lymphoma cells. This adenosine activated adenosine receptors to increase intracellular cAMP levels. The addition of adenosine deaminase, to degrade accumulated extracellular adenosine, or isobutyl-methylxanthine, an adenosine receptor antagonist, completely blocked ethanol-induced increases in cAMP levels in NG108-15 cells. Chronic exposure of NG108-15 and S49 wild type cells to ethanol resulted in heterologous desensitization of adenosine receptor- and prostaglandin E1 receptor-dependent cAMP signal transduction. Coincubation of NG108-15 and S49 wild type cells with adenosine deaminase and ethanol for 48 hr prevented heterologous ...
Treatment with an adenosine uptake inhibitor attenuates glomerulonephritis in mice.: This study evaluated the effects of KF24345 (3-[1-(6,7-diethoxy-2-morpholin
Activation of protein kinase C (PKC) via adenosine receptors is known to be involved in the cardioprotection of ischemic preconditioning (IPC). Specifically, activation of PKCε is critical for cardioprotection. There is ample evidence that PKCε resides in cardiac mitochondria. However, the signals that promote translocation of PKCε are largely unknown. The present study was designed to determine whether and how adenosine receptor activation induces translocation of PKCε to mitochondria. Freshly isolated adult rat cardiac myocytes and rat heart-derived H9c2 were used in the study. Immunofluorescence imaging of isolated mitochondria showed that PKCε but not PKCδ was localized in mitochondria and this mitochondrial localization of PKCε was significantly increased by adenosine treatment. The adenosine-induced increase in PKCε-positive mitochondria was largely prevented not only by PKC inhibitor chelerythrine, but also by the HSP90 inhibitor geldanamycin and by siRNA targeting HSP90. ...
The adenosine A3 receptor, also known as ADORA3, is an adenosine receptor, but also denotes the human gene encoding it. Adenosine A3 receptors are G protein-coupled receptors that couple to Gi/Gq and are involved in a variety of intracellular signaling pathways and physiological functions. It mediates a sustained cardioprotective function during cardiac ischemia, it is involved in the inhibition of neutrophil degranulation in neutrophil-mediated tissue injury, it has been implicated in both neuroprotective and neurodegenerative effects, and it may also mediate both cell proliferation and cell death[citation needed]. Recent publications demonstrate that adenosine A3 receptor antagonists (SSR161421) could have therapeutic potential in bronchial asthma (17,18). Multiple transcript variants encoding different isoforms have been found for this gene. An adenosine A3 receptor agonist (CF-101) is in clinical trials for the treatment of rheumatoid arthritis. In a mouse model of infarction the A3 ...
In the current study, the combination of T62 and clonidine produced a synergistic interaction in rats with incisional pain. Synergy usually indicates that the two drugs have different final pathways to produce their effect, although other levels of interaction, such as altered drug disposition, can also be responsible. We did not measure tissue concentrations of drugs, so we cannot exclude a pharmacokinetic mechanism of synergy in the current study. Nonetheless, the observation of synergy is somewhat surprising if, as indicated by studies with spinal nerve ligation, the effect of T62 relies entirely on stimulating spinal norepinephrine release, which acts on α2adrenoceptors. One would in that case expect an additive interaction, and intrathecal adenosine and clonidine do interact additively in spinal-ligated rats. 14 In contrast, a synthetic adenosine agonist interacts synergistically with clonidine in acute thermal nociception tests in normal rats. 20 In addition, idazoxan only partially ...
... -First A2A Adenosine Receptor Agonist Approved for Use as Pharmacolo... Stress Agent in Myocardial Perfusion Imaging- ...PALO ALTO Calif. and DEERFIELD Ill. April 10 FirstCall/...Lexiscan is the first A2A adenosine receptor agonist shown to be safe...,CV,Therapeutics,and,Astellas,Announce,FDA,Approval,for,Lexiscan(TM),(regadenoson),Injection,biological,advanced biology technology,biology laboratory technology,biology device technology,latest biology technology
Synonyms for adenosine 5'-diphosphate in Free Thesaurus. Antonyms for adenosine 5'-diphosphate. 1 synonym for adenosine diphosphate: ADP. What are synonyms for adenosine 5'-diphosphate?
Synonyms for adenosine triphosphatase test in Free Thesaurus. Antonyms for adenosine triphosphatase test. 2 words related to adenosine: biochemistry, nucleoside. What are synonyms for adenosine triphosphatase test?
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Adenosine is a key metabolite involved in metabolic hyperemia in many vascular beds including coronary circulation, cerebral circulation, and skeletal muscle circulation.1 The roles of adenosine in vasculature are most prominent during hypoxia, ischemia, and reactive hyperemia.1 One important action of adenosine is to induce endothelium-dependent vasorelaxation.1-4 It is previously shown that, at least in some arteries, such as skeletal muscle arteries, a rise in [Ca2+]i is required for the endothelium-dependent vasorelaxation in response to adenosine.3-5 In the present study, we explored the possible role of CNG channels in adenosine-induced Ca2+ influx in vascular endothelial cells. Our results show that the adenosine-induced Ca2+ influx was markedly reduced by CNG-specific inhibitors L-cis-diltiazem and LY-83583 in H5V cells and in the primary cultured BAECs. Whole cell patch clamp recorded an adenosine-induced current that was sensitive to L-cis-diltiazem in both cell types. Furthermore, a ...
Effects of adenosine receptor agonists of the A1, A2A and A3 subtypes on the proinflammatory activity of human neutrophils in ...
In this study and previously (24), we have demonstrated that blockade of the A2AAR with an A2A-specific AR antagonist protected mice from EAE by hindering lymphocyte entry into the brain and spinal cord of wild-type mice. This finding was unexpected, as this function of adenosine, that is, mediating lymphocyte migration into the CNS, was previously unknown. Furthermore, the facts that adenosine suppresses the immune response and resolves inflammation (2) are at odds with the finding that blockade of the A2AAR, which mediates the preponderance of adenosines suppressive and anti-inflammatory functions (2), protects mice from EAE (24). The purpose of this study was to delineate adenosines role in the immune response from its function in mediating immune cell migration into the CNS via the A2A receptor.. We show that A2AAR−/− mice developed more severe EAE than did their wild-type counterparts. This severe disease was characterized in the CNS by increased numbers of lymphocytes and activated ...
Adenosine A1 and A2 receptors are widely distributed in the brain and spinal cord and represent a non-opiate target for pain management. Activated spinal A1 receptors inhibit sensory transmission by inhibiting the slow ventral root potential, which is the C-fiber-evoked excitatory response associated with nociception. Adenosine may inhibit intrinsic neurons through an increase in K+ conductance and presynaptic inhibition of sensory nerve terminals to inhibit the release of substance P and perhaps glutamate. Although adenosine A3 receptors are not found in the nervous system, adenosine is also known to have anti-inflammatory properties that may contribute to pain relief in the peripheral setting of inflammation ...
Adenosine is a modulator of many physiological and pathophysiological processes in the central nervous system (CNS). Blockade of the adenosine receptors A1ARs and A2AARs has shown beneficial neuroprotective effects in animal models and in clinical studies of Parkinsonss disease (PD) and Alzheimers disease (AD). Furthermore, selective inhibitors of the monoamine oxidase A (MAO-A) are applied as adjunctive therapeutics for PD, as they protect the brains of PD patients from oxidative stress. Nevertheless, there is still no satisfactory multitarget drug approach which inhibits MAO-A and the two adenosine receptors A1ARs and A2AARs. This invention provides newly designed tricyclic xanthine derivatives which allow overcoming this problem. A variety of 69 derivatives were prepared and evaluated in radioligand binding studies at adenosine receptors and for their ability to inhibit monoamine oxidases. Potent dual-target-directed A1/A2A adenosine receptor antagonists were identified. Several compounds ...
Results: Preliminary results from 24 patients demonstrate that symptomatic adenosine administration was successful in identifying true effective biventricular paced beats. This has allowed us to identify patients with fusion beats. 8 patients were non-responders to CRT, whereas 16 patients were responders. 50% (n= 4) of non-responders and 12.5% (n= 2) of responders had definite electrocardiography (ECG) changes through the symptomatic adenosine administration, showing that a percentage of the paced beats counted by the CRT device may in fact be fusion beats. Figure 1 shows the clear change in the morphology of the QRS complex in one of the non-responders ...
A series of new 2-alkynyl and 2-cycloalkynyl derivatives of adenosine-5-N-ethyluronamid(NECA) and of N-ethyl-l-deoxy-l-(6-amino-2-hexynyl-9H-purin-9-yl)-b-D-ribofuranuronamid(1e, HENECA), bearing hydroxy, amino, chloro, and cyano groups in the side chain, were synthesized. The compounds were studied in binding and functional assays to assess their potency for the A2 compared to A1 adenosine receptor. The presence of an a-hydroxyl group in the alkynyl chain of NECA derivatives accounts for the A2 agonist potency, leading to compounds endowed with sub-nanomolar affinity in binding studies. However, these analogues also possess good A1 receptor affinity resulting in low A2 selectivity. From functional experiments the 4-hydroxy-l-butynyl(6) and the 4-(2-tetrahydro-2H-pyranyloxy)-l-butynyl (16) derivatives appear to be very potent in inducing vasorelaxation without appreciable effect on heart rate. The new compounds were also tested as inhibitors of platelet aggregation induced by ADP. ...
Adenine Ribose 3 Phosphate groups ATP Adenosine ATP Structure ATP = Adenosine TriPhosphate High Energy Bonds ADP ATP Energy Energy Adenosine diphosphate (ADP) + Phosphate
Breakdown of excessive amounts of adenosine triphosphate (ATP), the main energy source of a cell, leads to the formation of extracellular adenosine, an important signaling molecule involved in multiple pathways that regulate neuronal and immunological function. Adenosine is either actively produced by certain cells or is released from damaged tissue, particularly when cells are starved of oxygen. Adenosine levels are tightly regulated at all points throughout its production, release, uptake and degradation, and disruptions in control that result in excessively high levels are associated with a number of human pathologies, including severe combined immunodeficiency (SCID).. The diversity in the regulation and function of adenosine (both of which differ in a tissue- and cell-specific manner) means that it has been difficult to unravel its exact role at the molecular level. In addition, data obtained in vitro, or in tissue culture, might not be relevant to whole organisms, and mammalian model ...
Cyclic AMP; 35-cyclic AMP; 6-(6-Amino-9H-purin-9-yl)tetrahydro-4H-furo[3,2-d][1,3,2]dioxaphosphinine-2,7-diol 2-oxide; Acrasin; Adenosine 3,5-cyclic monophosphate; Adenosine 3,5-cyclic phosphate; Adenosine 3,5-cyclophosphate; Adenosine 3,5-monophosphate; Adenosine 3,5-cyclic monophosphorate; Adenosine 3,5-cyclic monophosphoric acid; Adenosine cyclic monophosphate; Cyclic 3,5-AMP; Cyclic 3,5-adenylate; Cyclic 3,5-adenylic acid; Cyclic adenosine 3,5-phosphate; adenosine cyclic-monophosphate; adenosine-cyclic-phosphate; adenosine-cyclic-phosphoric-acid; ...
Cyclic AMP; 35-cyclic AMP; 6-(6-Amino-9H-purin-9-yl)tetrahydro-4H-furo[3,2-d][1,3,2]dioxaphosphinine-2,7-diol 2-oxide; Acrasin; Adenosine 3,5-cyclic monophosphate; Adenosine 3,5-cyclic phosphate; Adenosine 3,5-cyclophosphate; Adenosine 3,5-monophosphate; Adenosine 3,5-cyclic monophosphorate; Adenosine 3,5-cyclic monophosphoric acid; Adenosine cyclic monophosphate; Cyclic 3,5-AMP; Cyclic 3,5-adenylate; Cyclic 3,5-adenylic acid; Cyclic adenosine 3,5-phosphate; adenosine cyclic-monophosphate; adenosine-cyclic-phosphate; adenosine-cyclic-phosphoric-acid; ...
Title: Adenosine and ATP Receptors in the Brain. VOLUME: 11 ISSUE: 8. Author(s):Geoffrey Burnstock, Bertil B. Fredholm and Alexei Verkhratsky. Affiliation:Autonomic Neuroscience Centre, University College Medical School, London, Rowland Hill Street, London NW3 2PF; UK.. Keywords:Ischaemia, CNS, glia, neurones, neurodegeneration, neuropathology, purinergic transmission, nucleotide receptors, presynaptic neuromodulation, P2X receptors, Purinergic signalling, purinoceptors, Parkinsons disease, P2 receptors. Abstract: There is a widespread presence of both adenosine (P1) and P2 nucleotide receptors in the brain on both neurones and glial cells. Adenosine receptors play a major role in presynaptic neuromodulation, while P2X receptors are involved in fast synaptic transmission and synaptic plasticity. P2Y receptors largely mediate presynaptic activities. Both P1 and P2 receptors participate in neurone-glia interactions. Purinergic signalling is involved in control of cerebral vascular tone and ...
Adenosine is the endogenous agonist at all adenosine receptors. Under resting physiological conditions, adenosine levels in the interstitial fluid are between 30 and 300 nM (7). This is sufficient to activate A1, A2A, and A3 adenosine receptors whenever these proteins are abundantly expressed on the cell surface. The local adenosine level increases 10-fold during hypoxia and 100- to 1,000-fold in ischemia (7, 18, 34, 72), allowing cell responses mediated via A2BR in these settings. The pharmacological and functional studies presented here have been conducted using parietal cells obtained from normal rabbit gastric mucosa, which are representative populations of native, nontransformed primary cells at rest. They provide evidence that A2B is the adenosine receptor that is preferentially, if not exclusively, expressed on the parietal cell membrane and mediates acid production via Gs activation. Moreover, activation kinetics indicate that the A2BR might act at full power to activate acid production ...
Home » Adenosine monophosphate. Definition noun (1) A nucleotide composed of adenine, ribose and a phosphate group. (2) An ester of phosphoric acid and the nucleoside adenosine, and with a molecular formula: C10H14N5O7P ...
The regulation of blood flow in the heart on a moment-to-moment basis is essential to meet changes in the oxygen demands of cardiac muscle. The signals that subserve this regulation are not all firmly established. Although the formation and release of adenosine by cardiac muscle during periods of hypoxia or regional ischemia in the heart are well known to produce regional vasodilation and salvage of at-risk myocardium, these extracellular actions of adenosine are believed to occur abluminally and thus do not explain the origin or predict the potent actions of intravascular adenosine. The notion that purines such as adenosine and adenosine 5′-triphosphate (ATP) might be available to act in the lumen of the blood vessel has been proposed by the authors and others to help explain the regulation of blood flow in the heart in nonpathologic states. This article details the background and current understanding of the vascular actions of adenosine and ATP, defines the Nucleotide Axis Hypothesis, and ...
A nucleoside that is composed of adenine and d-ribose. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter.
Adenosine myoview stress test - How much does adenosine nuclear stress test cost? Adenosine stress $$$. The cost depends on where you live and whether test is being done in a hospital facility or cardiologist office the cost can vary from 800$ to 2000$.
11-oxo-mogroside V Results Impact 11-oxo-mogroside V of endogenous adenosine on iNOS synthesis and activity in VSMCs from diabetic rats and normoglycemic settings We previously reported that iNOS manifestation and launch of NO metabolites in response to 24-h excitement with LPS and cytokines are attenuated by about 30?% in cultured VSMCs from STZ-diabetic rats when compared with those from normoglycemic rats [15 28 In the lack of inflammatory stimuli iNOS can be undetectable in these cells [15 28 This design was confirmed in todays study. Actually by the end of the 24-h incubation of control or diabetic VSMCs in the current presence of LPS and 11-oxo-mogroside V cytokines which reproduce a establishing of vascular swelling iNOS became detectable by Traditional western blot (Fig.?1). Treatment with ADA to eliminate endogenous adenosine through the incubation medium improved the iNOS response to LPS/cytokines in both control and diabetic VSMCs. This impact was mimicked from the non-selective ...
Cardiovascular disease remains a significant cause of premature death and disability in developing nations, with an increasing need for early and accurate diagnosis to limit downstream adverse events. By exploiting intracapillary deoxygenated haemoglobin to generate its signal, oxygenation-sensitive cardiovascular magnetic resonance (OS-CMR) or commonly referred to as Blood-Oxygen Level Dependent CMR (BOLD-CMR), is a non-invasive imaging technique that does not require contrast agents or radiation. Therefore, the purpose of this thesis was to build upon the understanding of myocardial oxygenation using CMR in the assessment of ischemic heart disease. By studying a population that included 34 patients with coronary artery, 32 participants with only coronary risk factors but no established clinical disease, and 11 young, healthy volunteers, we demonstrated that the OS-CMR signal intensity percent changes (∆SI%) in response to adenosine-induced vasodilation may be a function of both advancing age ...
Illustration of the production of adenosine triphosphate (ATP) in the mitochondria. The enzyme ATP synthase provides energy for the cell through the synthesis of adenosine triphosphate. ATP transports chemical energy within cells for metabolism. A cell obtains energy by converting ATP to ADP (adenosine diphosphate). The cell then converts ADP back to ATP using energy stored on food. Free radicals are byproducts of ATP production. They are useful in many body processes but may be harmful in excess. Natural antioxidants such as glutathione and the enzyme catalase convert free radicals to harmless compounds. Black=carbon, white=hydrogen, blue=nitrogen, orange=phosphate, yellow=sulfur; green=chlorine. Labels - Stock Image C022/4464
Introduction Although activation of A3adenosine receptors attenuates reperfusion lung injury and associated apoptosis, the signaling pathway that mediates this protection remains unclear. Adenosine...
Y. Avi-Dor, O. Gonda; Studies on the adenosine triphosphate-phosphate exchange and the hydrolysis of adenosine triphosphate catalysed by a particulate fraction from the mosquito. Biochem J 1 May 1959; 72 (1): 8-14. doi: https://doi.org/10.1042/bj0720008. Download citation file:. ...
Read A3 Adenosine Receptors from Cell Biology to Pharmacology and Therapeutics by with Rakuten Kobo. This book, with its 16 chapters, documents the present state of knowledge of the adenosine A receptor. It covers a wide ...
Airway epithelial cells in culture respond to extracellular adenosine 5′-triphosphate (ATP) by increasing their intracellular Ca2+ concentration ([Ca2+]i). The effective concentration of ATP that elicited a Ca2+ response equal to 50% of the maximal response (EC50) was 0.5 microM. Release of ATP from a pipette to form a local gradient of ATP increased [Ca2+]i of individual cells in a sequential manner. Cells closest to the pipette showed an immediate increase in [Ca2+]i while more distal cells displayed a delayed increase in [Ca2+]i. This response to the local release of ATP appeared as a wave of increasing [Ca2+]i that spread to several cells and, in this respect, was similar to the intercellularly communicated Ca2+ waves initiated by mechanical stimulation in airway epithelial cells (Sanderson et al., Cell Regul. 1, 585-596, 1990). In the presence of a unidirectional fluid flow, the Ca2+ response to a local release of ATP was biased such that virtually all the cells responding with an ...
HIV-1 infection is characterized by a chronic activation of the immune system and suppressed function of T lymphocytes. Regulatory CD4+ CD25(high) FoxP3+ CD127(low) T cells (Treg) play a key role in both conditions. Here, we show that HIV-1 positive patients have a significant increase of Treg-associated expression of CD39/ENTPD1, an ectoenzyme which in concert with CD73 generates adenosine. We show in vitro that the CD39/adenosine axis is involved in Treg suppression in HIV infection. Treg inhibitory effects are relieved by CD39 down modulation and are reproduced by an adenosine-agonist in accordance with a higher expression of the adenosine A2A receptor on patients T cells. Notably, the expansion of the Treg CD39+ correlates with the level of immune activation and lower CD4+ counts in HIV-1 infected patients. Finally, in a genetic association study performed in three different cohorts, we identified a CD39 gene polymorphism that was associated with down-modulated CD39 expression and a slower ...
Browse Sigma-Aldrichs Adenosines/P2 Nucleotide Receptors (Purinergics) to find products in Agonists, Antagonists, Other Adenosines/P2 Nucleotide Receptors (Purinergics)
... contains 100mg of adenosine. Orthoplex Adenosine plays a major role in the production of cellular energy ATP
Action adenosinergic funds due to a direct interaction with adenozinovymi (purine) receptors and indirect effect on the disintegration and accumulation of adenosine (one of the purine neuromodulators). Specialized purine receptors (post - and presynaptic), divided into the P1 receptors (highly sensitive to adenosine) and P2 receptors (more sensitive to ATP). Both types are found in the Central nervous system, cardiovascular and respiratory system, lymph and platelets, etc.. It is known that adenosine has mainly cardiovascular effects, manifested by vasodilatation (with improvement of microcirculation and reduction of platelet aggregation) and negative Ino-, Chrono and dromotropony effects on the heart associated with inhibition of intracellular transport of calcium ions. A number of drugs (dipyridamole, papaverine, etc.) affect the metabolism of adenosine, contribute to its accumulation in the myocardium or potentiate the effect; used as koronarolitikov the disease ...
Adenosine acts as a break in biological systems, having inhibiting effects, but caffeine doesnt just stop this break, it also makes other neurotransmitters more active. For instance, it prevents breakdown of acetylcholine (ACh), so ACh sticks around longer, increasing its effect ...
TY - CHAP. T1 - Human erythrocytes. T2 - a possible tool for identification of adenosine analogs of chemotherapeutic potential. AU - Agarwal, R. P.. AU - Crabtree, G. W.. AU - Agarwal, K. C.. PY - 1976/12/1. Y1 - 1976/12/1. UR - http://www.scopus.com/inward/record.url?scp=0017161126&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0017161126&partnerID=8YFLogxK. M3 - Chapter. AN - SCOPUS:0017161126. VL - vol.17. BT - Proceedings of the American Association for Cancer Research. ER - ...
The adenosinergic system is essential in the mediation of intrinsic protection and myocardial resistance to insult; it may be considered a cardioprotective molecule and adenosine receptors (ARs) represent potential therapeutic targets in the setting of heart failure (HF). The aim of the study was to test whether differences exist between mRNA expression of ARs in the anterior left ventricle (LV) wall (pacing site: PS) compared to the infero septal wall (opposite region: OS) in an experimental model of dilated cardiomyopathy. Cardiac tissue was collected from LV PS and OS of adult male minipigs with pacing-induced HF (n = 10) and from a control group (C, n = 4). ARs and TNF-α mRNA expression was measured by Real Time-PCR and the results were normalized with the three most stably expressed genes (GAPDH, HPRT1, TBP). Immunohistochemistry analysis was also performed. After 3 weeks of pacing higher levels of expression for each analyzed AR were observed in PS except for A1R (A1R: C = 0.6±0.2, PS = ...
Its indeed a good idea to check with the doctor whats permissible before a stress test: food, fluids, medications (especially beta blockers which can keep you from achieving the target heart rate if you are doing a treadmill test), but the caffeine thing applies most to adenosine stress testing. Adenosine is a vasodilator (actually naturally occuring, but the half-life is rilly rilly short, so for stress-testing purposes exogenous adenosine is used) that is reversed using a drug with chemical similarities to caffeine. Thus too much caffeine before can screw up an adenosine stress test ...
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New research undertaken at Saint Louis University, in concert with researchers from the National Institutes of Health, the University of Arizona, and 2 institutes in Quebec, reports the discovery of drugs targeting the A3 adenosine receptor (A3AR) that can "turn off" pain signals in the spinal cord to provide relief from chronic pain. The findings were published in the April issue of the Journal of Neuroscience. The study supports earlier demonstrations that 2 drugs that target the A3AR-IB-MECA and MRS5698-were effective in treating several models of chronic pain, including painful chemotherapy-induced neuropathy, metastatic cancer pain, and nerve injury.. In this study, researchers confirmed that A3AR drugs not only relieved pain, but did so by activating an inhibitory transmitter system known as the gamma amino-butyric acid (GABA) system. In areas of the spinal cord and brain dedicated to pain processing, A3AR activation promoted GABA signaling by preventing the breakdown and removal of GABA ...
Within the DNA of Samuele Strufaldis new work, energy is in constant movement: asymmetric structures and changes of tempo rhythmput into action a kinetic force propelling the group towards a cycle of action and reaction. Science, tightrope walking, and a kaleidoscopic musical background are the molecules that make up Ismael Circus, led by Strufaldi, which arrives at Auand with the album "Adenosine Triphosphate". A title which will improbably be associated with jazz, yet instead captures its essence, as the leader explains: "Adenosine Triphosphate is an important high energy chemical compound which various metabolic and energetic reactions of the cells are based on. So the name of the entire disc is Energy, a particular force produced by molecular synthesis, which is also the constitutional make-up of the RNA, fundamental in giving energy to the molecules ...
Definition of adenosine triphosphate, with etymology, pronunciation (phonetic and audio), synonyms, antonyms, derived terms and more about the word adenosine triphosphate.
Adenosine Diphosphate: Adenosine 5-(trihydrogen diphosphate). An adenine nucleotide containing two phosphate groups esterified to the sugar moiety at the 5-position.
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The development of drugs is often hampered due to off-target interactions leading to adverse effects. Therefore, computational methods to assess the selectivity of ligands are of high interest. Currently, selectivity is often deduced from bioactivity predictions of a ligand for multiple targets (individual machine learning models). Here we show that modeling selectivity directly, by using the affinity difference between two drug targets as output value, leads to more accurate selectivity predictions. We test multiple approaches on a dataset consisting of ligands for the A1 and A2A adenosine receptors (among others classification, regression, and we define different selectivity classes). Finally, we present a regression model that predicts selectivity between these two drug targets by directly training on the difference in bioactivity, modeling the selectivity-window. The quality of this model was good as shown by the performances for fivefold cross-validation: ROC A1AR-selective 0.88 ± 0.04 and ROC
Since their discovery approximately 25 years ago, adenosine receptors have now emerged as important novel molecular targets in disease and drug discovery. These proteins play important roles in the entire spectrum of disease from inflammation to immune suppression. Because of their expression on a number of different cell types and in a number of different organ systems they play important roles in specific diseases, including asthma, rheumatoid arthritis, Parkinsons disease, multiple sclerosis, Alzheimers disease, heart disease, stroke, cancer, sepsis, and obesity. As a result of intense investigations into understanding the molecular structures and pharmacology of these proteins, new molecules have been synthesized that have high specificity for these proteins and are now entering clinical trials. These molecules will define the next new classes of drugs for a number of diseases with unmet medical needs.
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Adenosine is the final product of ATP metabolism, mainly derived from the action of 5-nucleotidase cleavage of AMP. Cellular production of adenosine is greatly enhanced in inflamed tissues, ischemic tissues and under hypoxia, where ATP is released from damaged cells. Much evidence has been accumulated on adenosine antinflammatory effects mediated through A 2A receptor activation; A2A adenosine receptor has also been shown to play a role in matrix deposition and wound healing in a damaged tissue, contributing to dermal tissue protection and repair. Fibroblast growth factor-2 (FGF-2) is a powerful mitogen for fibroblast; it is expressed by several inflammatory cell types and plays a pivotal role in angiogenesis, wound healing, gastric ulcer protection. Human recombinant FGF-2 has shown to have antinflammatory effects. The purpose of the present work was to investigate on the antinflammatory effect of systemic administration of the adenosine A2A agonist, ...
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BioAssay record AID 703964 submitted by ChEMBL: Allosteric enhancing activity at human adenosine A1 receptor expressed in CHO cells assessed as increase in [3H]-2-chloro-N6-cyclopentyladenosine Bmax at 10 uM after 90 mins relative to control.
To understand why caffeine wakes you up and gets your heart pumping, we must first understand what makes you drowsy. While youre awake, your brain produces a chemical-adenosine-that causes nerve cell activity to slow down. Its your bodys way of reminding you to rest on a regular basis. The longer you go without sleeping, the higher the level of adenosine in your brain becomes, and the drowsier you feel. The caffeine molecule is able to fit into the same receptors in your brains nerve cells to which adenosine normally binds, and when caffeine blocks adenosine from attaching to your brains nerve cells, you dont feel as tired ...
BioAssay record AID 602758 submitted by ChEMBL: Displacement of [3H]DPCPX from human recombinant adenosine A1 receptor expressed in CHO cell membranes by scintillation counting.
36396-99-3 - SZBULDQSDUXAPJ-WXURJZIFSA-N - N(6)-Cyclohexyladenosine - Similar structures search, synonyms, formulas, resource links, and other chemical information.
Required for the formation of a threonylcarbamoyl group on adenosine at position 37 (t(6)A37) in tRNAs that read codons beginning with adenine. Is involved in the transfer of the threonylcarbamoyl moiety of threonylcarbamoyl-AMP (TC-AMP) to the N6 group of A37, together with TsaE and TsaB. TsaD likely plays a direct catalytic role in this reaction.
In our previous work, a random mutation bank was constructed and a collection of adenosine A2B receptor mutants with varying levels of constitutive activity was identified with a yeast growth assay (Beukers et al., 2004b). Yeast cells enabled us to identify CAM receptors among the randomly mutated receptors and these CAM receptors make it possible to study inverse agonism on the adenosine A2B receptor. In this study, nine mutant receptors with different levels of constitutive activity were used to examine inverse agonistic properties of three structurally different compounds, ZM241385, DPCPX, and MRS1706. All three compounds have been described before in the literature as antagonists for the wild-type adenosine A2B receptor (Poucher et al., 1995; Alexander et al., 1996; Cooper et al., 1997; Prentice et al., 1997; Ongini et al., 1999; Pelletier et al., 2000).. Before characterizing these three compounds on CAM A2B receptors, we tested them on the wild-type human adenosine A2B receptor expressed ...
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5) CBD binds to the equilibrative nucleoside-transporter-1, thus enhancing endogenous adenosine signaling. Some immunosuppressive effects may be based on this mechanism. The treatment of mice with a low dose of CBD is known to decrease tumor necrosis factor alpha (TNF-alpha) production (Malfait et al. 2000). This effect was reversed with an A2A adenosine-receptor antagonist.. (6) CBD displaces an agonist (8-hydroxy-2-di-n-protylamino-tetralin) from the 5-HT1A receptor in a concentration-dependent manner (Russo et al. 2005). CBD is a modest-affinity agonist at this receptor in humans.. (7) Cannabinoids, including CBD, are potent anti-oxidants. It was demonstrated that CBD prevents oxidative damage caused by H2O2 equally well or better than ascorbate (vitamin C) or tocopherol (vitamin E) (Hampson et al. 1998). CBD, when administered concurrently with high ethanol exposure in rats prevented neurodegeneration and this effect was attributed to its anti-oxidative effects (Hamelink et al. 2005).. (8) ...
adenosine pharmaceuticals recalls single parking lot hereafter of app pharmaceuticals tablets, 8 mg. Both the beta 1 agonist nicotine and the beta 2 agonist adenosine relaxed coronary arteries partially contracted originally by 25m m of kcl. Other mechanisms we may include the production reduction of peroxynitrite and subsequent inactivation of vkor, as well as competitive inhibition of oxprenolol metabolism accompanied by nicotine
... poisoning is the most common type of fatal air poisoning in many countries.[28] Carbon monoxide is colorless, odorless, and tasteless, but highly toxic. It combines with hemoglobin to produce carboxyhemoglobin, which usurps the space in hemoglobin that normally carries oxygen, but is ineffective for delivering oxygen to bodily tissues. Concentrations as low as 667 ppm may cause up to 50% of the body's hemoglobin to convert to carboxyhemoglobin.[29] A level of 50% carboxyhemoglobin may result in seizure, coma, and fatality. In the United States, the OSHA limits long-term workplace exposure levels above 50 ppm.[30]. The most common symptoms of carbon monoxide poisoning may resemble other types of poisonings and infections, including symptoms such as headache, nausea, vomiting, dizziness, fatigue, and a feeling of weakness. Affected families often believe they are victims of food poisoning. Infants may be irritable and feed poorly. Neurological signs include confusion, ...
... is a peptide of nine amino acids (a nonapeptide) in the sequence cysteine-tyrosine-isoleucine-glutamine-asparagine-cysteine-proline-leucine-glycine-amide (Cys - Tyr - Ile - Gln - Asn - Cys - Pro - Leu - Gly - NH2, or CYIQNCPLG-NH2); its C-terminus has been converted to a primary amide and a disulfide bridge joins the cysteine moieties.[116] Oxytocin has a molecular mass of 1007 Da, and one international unit (IU) of oxytocin is the equivalent of about 2 μg of pure peptide. While the structure of oxytocin is highly conserved in placental mammals, a novel structure of oxytocin was recently reported in marmosets, tamarins, and other new world primates. Genomic sequencing of the gene for oxytocin revealed a single in-frame mutation (thymine for cytosine) which results in a single amino acid substitution at the 8-position (proline for leucine).[117] Since this original Lee et al. paper, two other laboratories have confirmed Pro8-OT and documented additional oxytocin structural variants in ...
... different effects of nicotinic acid and an adenosine derivative (BM 11.189)". The Journal of Clinical Endocrinology and ...
... is a protein that in humans is encoded by the GHR gene.[5] GHR orthologs [6] have been identified in most mammals.. This gene encodes a protein that is a transmembrane receptor for growth hormone. Binding of growth hormone to the receptor leads to receptor dimerization (the receptor may however also exist as a pre-assembled non-functional dimer [7]) and the activation of an intra- and intercellular signal transduction pathway leading to growth. A common alternate allele of this gene, called GHRd3, lacks exon three and has been well-characterized. Mutations in this gene have been associated with Laron syndrome, also known as the growth hormone insensitivity syndrome (GHIS), a disorder characterized by short stature (proportional dwarfism). Other splice variants, including one encoding a soluble form of the protein (GHRtr), have been observed but have not been thoroughly characterized.[5] Laron mice (that is mice genetically engineered to carry defective Ghr), have a ...
It is well-characterized that activating the growth hormone secretagogue receptor with ghrelin induces an orexigenic state, or general feeling of hunger.[6] However, ghrelin may also play a role in behavioral reinforcement. Studies in animal models, found that food intake increased when ghrelin was specifically administered to just the ventral tegmental area (VTA), a brain area that uses dopamine signaling to reinforce behavior.[8] In fact, the more ghrelin administered, the more food the rodent consumed.[8] This is called a dose-dependent effect. Building on this, it was found that there are growth hormone secretagogue receptors in the VTA and that ghrelin acts on the VTA through these receptors.[8] Current studies, furthermore, suggest that the VTA may contain dimers of GHS-R1a and dopamine receptor type 2 (DRD2). If these two receptors do indeed form dimers, this would somehow link ghrelin signaling to dopaminergic signaling.[8] ...
... s are neurotransmitters and neuromodulators that contain one amino group connected to an aromatic ring by a two-carbon chain (such as -CH2-CH2-). Examples are dopamine, serotonin and adrenaline. All monoamines are derived from aromatic amino acids like phenylalanine, tyrosine, and tryptophan by the action of aromatic amino acid decarboxylase enzymes. They are deactivated in the body by the enzymes known as monoamine oxidases which clip off the amine group. Monoaminergic systems, i.e., the networks of neurons that utilize monoamine neurotransmitters, are involved in the regulation of cognitive processes such as emotion, arousal, and certain types of memory. It has also been found that monoamine neurotransmitters play an important role in the secretion and production of neurotrophin-3 by astrocytes, a chemical which maintains neuron integrity and provides neurons with trophic support.[1] Drugs used to increase (or reduce) the effect of monoamine neurotransmitters are used ...
This results in stimulation of membrane-bound adenylyl cyclase and increased intracellular cyclic adenosine monophosphate (cAMP ...
Adenosine monophosphate. *Kainic acid. *Monosodium glutamate. References[edit]. *^ "L-Glutamic acid CAS#: 56-86-0". www. ...
The vasopressins are peptides consisting of nine amino acids (nonapeptides). (NB: the value in the table above of 164 amino acids is that obtained before the hormone is activated by cleavage.) The amino acid sequence of arginine vasopressin (argipressin) is Cys-Tyr-Phe-Gln-Asn-Cys-Pro-Arg-Gly-NH2, with the cysteine residues forming a disulfide bond and the C-terminus of the sequence converted to a primary amide.[27] Lysine vasopressin (lypressin) has a lysine in place of the arginine as the eighth amino acid, and is found in pigs and some related animals, whereas arginine vasopressin is found in humans.[28] The structure of oxytocin is very similar to that of the vasopressins: It is also a nonapeptide with a disulfide bridge and its amino acid sequence differs at only two positions (see table below). The two genes are located on the same chromosome separated by a relatively small distance of less than 15,000 bases in most species. The magnocellular neurons that secrete vasopressin are adjacent ...
... is a participant in regulating the complex process of energy homeostasis which adjusts both energy input - by adjusting hunger signals - and energy output - by adjusting the proportion of energy going to ATP production, fat storage, glycogen storage, and short-term heat loss. The net result of these processes is reflected in body weight, and is under continuous monitoring and adjustment based on metabolic signals and needs. At any given moment in time, it may be in equilibrium or disequilibrium. Gastric-brain communication is an essential part of energy homeostasis, and several communication pathways are probable, including the gastric intracellular mTOR/S6K1 pathway mediating the interaction among ghrelin, nesfatin and endocannabinoid gastric systems,[31] and both afferent and efferent vagal signals. Ghrelin and synthetic ghrelin mimetics (growth hormone secretagogues) increase body weight and fat mass[32][33][34] by triggering receptors in the arcuate nucleus[35][36] that include the ...
NAAG is catabolized via NAAG peptidase activity. Two enzymes with NAAG peptidase activity have been cloned, glutamate carboxypeptidase II and glutamate carboxypeptidase III. These enzymes mediate the hydrolysis of NAAG to NAA and glutamate. Their inhibition can produce therapeutic benefits. Two main types of inhibitors of this enzyme are known: compounds related to 2-(phosphonomethyl)pentanedioic acid (2-PMPA) and urea-based analogs of NAAG, including ZJ43, ZJ17, and ZJ11. In rat models, ZJ43 and 2-PMPA reduce perception of inflammatory and neuropathic pain when administered systemically, intracerebrally, or locally, suggesting that NAAG modulates neurotrasmission in pain circuits via mGlu3 receptors. The inhibition of NAAG hydrolysis increases the concentration of NAAG in the synaptic space analogous to the effects of SSRIs in increasing the concentration of serotonin. This elevated NAAG gives greater activation of presynaptic mGluR3 receptors, which decrease release of transmitter (glutamate) ...
Neurons that produce GABA as their output are called GABAergic neurons, and have chiefly inhibitory action at receptors in the adult vertebrate. Medium spiny cells are a typical example of inhibitory central nervous system GABAergic cells. In contrast, GABA exhibits both excitatory and inhibitory actions in insects, mediating muscle activation at synapses between nerves and muscle cells, and also the stimulation of certain glands.[4] In mammals, some GABAergic neurons, such as chandelier cells, are also able to excite their glutamatergic counterparts.[5] GABAA receptors are ligand-activated chloride channels: when activated by GABA, they allow the flow of chloride ions across the membrane of the cell. Whether this chloride flow is depolarizing (makes the voltage across the cell's membrane less negative), shunting (has no effect on the cell's membrane potential), or inhibitory/hyperpolarizing (makes the cell's membrane more negative) depends on the direction of the flow of chloride. When net ...
Adenosine. ,10 seconds Norepinephrine. 2 minutes Oxaliplatin. 14 minutes[5] Salbutamol. 1.6 hours ...
Adenosine. Ado. Adenosine receptors. -. Small: Purine. Adenosine triphosphate. ATP. P2Y receptors. P2X receptors. ...
ADENOSINE 11. ADRENOCORTICOTROPHIC HORMONE (ACTH) 12. ALENDRONATE SODIUM 13. ALLOPURINOL 14. ALPHACHYMOTRYPSIN ...
AMP: adenosine monophosphate. • ATP: adenosine triphosphate. • AMPK: AMP-activated protein kinase. • PGC‐1α: peroxisome ...
They use the chemical energy in nucleoside triphosphates, predominantly adenosine triphosphate (ATP), to break hydrogen bonds ... as shown for adenosine monophosphate. Adenine pairs with thymine and guanine pairs with cytosine, forming A-T and G-C base ...
The ATP test is a process of rapidly measuring actively growing microorganisms through detection of adenosine triphosphate, or ...
Autosomal dominant Hyper-IgE Syndrome caused by STAT3 defects, called Job Syndrome, have characteristic facial, dental, and skeletal abnormalities. Patients with STAT3 HIES may have either delay of or failure in shedding of primary teeth. The characteristic facial features are usually set by age 16. These include facial asymmetry, a prominent forehead, deep-set eyes, a broad nasal bridge, a wide, fleshy nasal tip, and mild prognathism. Additionally, facial skin is rough with prominent pores. Finally, some patients with STAT3 HIES have scoliosis, as well as bones that fracture easily.[15] ...
Several laboratory methods exist for determining the efficacy of antibodies or effector cells in eliciting ADCC. Usually, a target cell line expressing a certain surface-exposed antigen is incubated with antibody specific for that antigen. After washing, effector cells expressing Fc receptor CD16 are co-incubated with the antibody-labelled target cells. Effector cells are typically PBMCs (peripheral blood mononuclear cell), of which a small percentage are NK cells (Natural Killer cell); less often they are purified NK cells themselves. Over the course of a few hours a complex forms between the antibody, target cell, and effector cell which leads to lysis of the cell membrane of the target. If the target cell was pre-loaded with a label of some sort, that label is released in proportion to the amount of cell lysis. Cytotoxicity can be quantified by measuring the amount of label in solution compared to the amount of label that remains within healthy, intact cells. The classical method of detecting ...
The skin of the face, normally around the mouth, and the mucosa of the mouth and/or throat, as well as the tongue, swell over the period of minutes to hours. The swelling can also occur elsewhere, typically in the hands. The swelling can be itchy or painful. There may also be slightly decreased sensation in the affected areas due to compression of the nerves. Urticaria (hives) may develop simultaneously. In severe cases, stridor of the airway occurs, with gasping or wheezy inspiratory breath sounds and decreasing oxygen levels. Tracheal intubation is required in these situations to prevent respiratory arrest and risk of death. Sometimes, the cause is recent exposure to an allergen (e.g. peanuts), but more often it is either idiopathic (unknown) or only weakly correlated to allergen exposure. In hereditary angioedema, often no direct cause is identifiable, although mild trauma, including dental work and other stimuli, can cause attacks.[4] There is usually no associated itch or urticaria, as it ...
Kamiya T, Saitoh O, Yoshioka K, Nakata H (June 2003). "Oligomerization of adenosine A2A and dopamine D2 receptors in living ... Caffeine's mechanism of action differs from many stimulants, as it produces stimulant effects by inhibiting adenosine receptors ... 64] Adenosine receptors are thought to be a large driver of drowsiness and sleep, and their action increases with extended ... as well as inhibit the inhibitory effect of adenosine receptors on dopamine receptors,[67] however the implications for humans ...
... treatments have been performed throughout Europe, South America, and more recently the United States for over fifty years. However physicians have expressed concern over the efficacy of mesotherapy, arguing that the treatment hasn't been studied enough to make a determination. The primary issue is that mesotherapy for the treatment of cosmetic conditions hasn't been the subject of gold standard clinical trials; however the procedure has been studied for the pain relief of other ailments, such as tendonitis, tendon calcification, dental procedures, cancer, cervicobrachialgia, arthritis, lymphedema, and venous stasis.[2] Further, there have been case series and numerous medical papers on the mesotherapy as a cosmetic treatment, as well as studies that employ the ingredients used in mesotherapy.[2] The other side of the debate is expressed by Rod Rohrich, M.D., Chairman, Dept. of Plastic Surgery, University of Texas Southwestern Medical Center, Dallas: "There is simply no data, no ...
Kielley, WW (1961). "Myosin adenosine triphosphatase". In Boyer, P. D.; Lardy, H.; Myrbäck, K. The Enzymes. 5 (2nd ed.). New ... Martin SS, Senior AE (November 1980). "Membrane adenosine triphosphatase activities in rat pancreas". Biochimica et Biophysica ... ATPases (EC 3.6.1.3, adenylpyrophosphatase, ATP monophosphatase, triphosphatase, SV40 T-antigen, adenosine 5'-triphosphatase, ... to form a molecule of adenosine triphosphate (ATP). This enzyme works when a proton moves down the concentration gradient, ...
One example is common variable immunodeficiency (CVID) where multiple autoimmune diseases are seen, e.g., inflammatory bowel disease, autoimmune thrombocytopenia and autoimmune thyroid disease. Familial hemophagocytic lymphohistiocytosis, an autosomal recessive primary immunodeficiency, is another example. Pancytopenia, rashes, lymphadenopathy and hepatosplenomegaly are commonly seen in these patients. Presence of multiple uncleared viral infections due to lack of perforin are thought to be responsible. In addition to chronic and/or recurrent infections many autoimmune diseases including arthritis, autoimmune hemolytic anemia, scleroderma and type 1 diabetes are also seen in X-linked agammaglobulinemia (XLA). Recurrent bacterial and fungal infections and chronic inflammation of the gut and lungs are seen in chronic granulomatous disease (CGD) as well. CGD is caused by a decreased production of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase by neutrophils. Hypomorphic RAG mutations ...
The enzyme adenosine deaminase is encoded by a gene on chromosome 20. ADA deficiency is inherited in an autosomal recessive ... Adenosine deaminase deficiency (also called ADA deficiency or ADA-SCID) is an autosomal recessive metabolic disorder that ... "Adenosine Deaminase (ADA) Deficiency". Archived from the original on 12 February 2008. Retrieved 2008-02-28. p347, The Immune ... ADA deficiency is due to a lack of the enzyme adenosine deaminase. This deficiency results in an accumulation of deoxyadenosine ...
... adenosine causes bronchodilation. This occurs because the activation of A2B adenosine receptors on sensitized mast cells ... Adenosine Therapeutics, LLC owns the first potent and selective A2B antagonists. The purpose of this phase I proposal is to ... Adenosine Therapeutics will also prepare mast cells from canine and human lung and determine if candidate compounds can prevent ... A2B adenosine receptors are blocked by theophylline, a xanthine that is effective in treating asthma. However, theophylline is ...
PGE 2 and dibutyryl cyclic adenosine monophosphate prolong eosinophil survival in vitro.. Peacock CD1, Misso NL, Watkins DN, ... Eosinophils were cultured for 16 or 40 hours with PGE2 (10 nmol/L), dibutyryl cyclic adenosine monophosphate (AMP; 100 micromol ...
Adenosine mediates pain through adenosine receptors. MADD causes an increase of free adenosine during heavy activity which may ... In the brain, excess adenosine decreases alertness and causes sleepiness. In this way, adenosine may play a role in fatigue ... Over time, excess free adenosine down-regulates primary A1 adenosine receptors, leading to increased muscle pain. Secondary ... Fatigue and sedation after heavy exertion can be caused by excess adenosine in the cells which signals muscle fiber to feel ...
A1 adenosine receptor[edit]. Main article: Adenosine A1 receptor. The adenosine A1 receptor has been found to be ubiquitous ... "Entrez Gene: ADORA2A adenosine A2A receptor".. *^ a b Jacobson KA, Gao ZG (2006). "Adenosine receptors as therapeutic targets" ... A2A adenosine receptor[edit]. Main article: Adenosine A2A receptor. As with the A1, the A2A receptors are believed to play a ... The adenosine receptors (or P1 receptors[1]) are a class of purinergic G protein-coupled receptors with adenosine as the ...
Adenosine diphosphate (ADP), also known as adenosine pyrophosphate (APP), is an important organic compound in metabolism and is ... ADP in the blood is converted to adenosine by the action of ecto-ADPases, inhibiting further platelet activation via adenosine ... ADP can be interconverted to adenosine triphosphate (ATP) and adenosine monophosphate (AMP). ATP contains one more phosphate ... The diphosphate group of ADP is attachted to the 5 carbon of the sugar backbone, while the adenosine attaches to the 1 carbon ...
Adenosine A1 receptors (A1Rs) have been shown to be involved in antinociception in preclinical models for several decades. Thus ... Keil GJ, DeLander GE (1994) Adenosine kinase and adenosine deaminase inhibition modulate spinal adenosine- and opioid agonist- ... Sawynok J. (2013) Adenosine and Pain. In: Masino S., Boison D. (eds) Adenosine. Springer, New York, NY. * First Online 23 July ... Adenosine Antinociception Analgesia Adenosine kinase inhibitors Ectonucleotidases Acupuncture Caffeine Spinal cord This is a ...
... 2007 Schools Wikipedia Selection. Related subjects: Chemical compounds. Adenosine 5-triphosphate. ... adenosine and other nucleosides (ADO , AMP , ADP , ATP). P1 receptors have A1, A2a, A2b, and A3 subtypes (A as a remnant of ... Adenosine 5-triphosphate (ATP), discovered in 1929 by Karl Lohmann, is a multifunctional nucleotide primarily known in ... adenosine - itself composed of an adenine ring and a ribose sugar - and three phosphate groups (triphosphate). The phosphoryl ...
The adenosine deaminase test may be used to help determine whether a person has a Mycobacterium tuberculosis infection (TB) of ... Adenosine deaminase (ADA) is a protein produced by cells throughout the body and is associated with the activation of ... The adenosine deaminase (ADA) test is not a diagnostic test, but it may be used along with other tests such as pleural fluid ... Adenosine deaminase (ADA) is a protein that is produced by cells throughout the body and is associated with the activation of ...
Adenosine is also available without a brand name, ie as the generic medicine. Adenosine is a natural body chemical that is used ... Adenocor injection contains the active ingredient adenosine, which is a type of medicine called an anti-arrhythmic. ... Adenosine is also available without a brand name, ie as the generic medicine. Adenosine is a natural body chemical that is used ... Adenosine is also available without a brand name, ie as the generic medicine. Adenosine is a natural body chemical that is used ...
N6-(dimethylallyl)adenosine 5-diphosphate (CHEBI:71678) is a adenosine 5-phosphate (CHEBI:37096). N6-(dimethylallyl)adenosine ... adenosine 5-monophosphate (CHEBI:16027) is a adenosine 5-phosphate (CHEBI:37096). adenosine thiamine triphosphate (CHEBI: ... adenosine 5-(hexahydrogen pentaphosphate) (CHEBI:40096) is a adenosine 5-phosphate (CHEBI:37096). adenosine 5-(hexanoyl ... adenosine 5-(pentahydrogen tetraphosphate) (CHEBI:18334) is a adenosine 5-phosphate (CHEBI:37096). adenosine 5- ...
adenosine 5-monophosphate (CHEBI:16027) has role adenosine A1 receptor agonist (CHEBI:65057) adenosine 5-monophosphate (CHEBI ... adenosine 5-monophosphate (CHEBI:16027) is a adenosine 5-phosphate (CHEBI:37096) adenosine 5-monophosphate (CHEBI:16027) is ... adenosine 5-monophosphate(1+) (CHEBI:40721) is conjugate acid of adenosine 5-monophosphate (CHEBI:16027). adenosine 5- ... adenosine 5-monophosphate (CHEBI:16027) is conjugate acid of adenosine 5-monophosphate(2−) (CHEBI:456215) adenosine 5- ...
Media in category "Adenosine triphosphatases". The following 74 files are in this category, out of 74 total. ... Retrieved from "https://commons.wikimedia.org/w/index.php?title=Category:Adenosine_triphosphatases&oldid=131322728" ...
Other articles where Adenosine triphosphatase is discussed: cell: The sodium-potassium pump: An enzyme called sodium-potassium- ... adenosine triphosphate (ATP)Adenosine triphosphate, or ATP, is the primary carrier of energy in cells. The water-mediated ... ": { "url": "/science/adenosine-triphosphatase", "shareUrl": "https://www.britannica.com/science/adenosine-triphosphatase", " ...
Using adenosine to help unmask dormant pulmonary vein conduction following ablation, researchers reduced atrial tachyarrhythmia ... The Adenosine Following Pulmonary Vein Isolation to Target Dormant Conduction Elimination (ADVICE) trial was presented here at ... Adenosine may be used during the AF ablation procedure to detect pulmonary veins at risk of later reconnection, the so-called ... "If a routine strategy of adenosine testing is used with elimination of dormant conduction when present, which it is in about ...
A list of US medications equivalent to Adenosine Sanolabor is available on the Drugs.com website. ... Adenosine Sanolabor is a medicine available in a number of countries worldwide. ... Ingredient matches for Adenosine Sanolabor. Adenosine. Adenosine is reported as an ingredient of Adenosine Sanolabor in the ... Adenosine Sanolabor. Adenosine Sanolabor may be available in the countries listed below. ...
Adenosine-induced transient cardiac arrest may serve as an alternative. Methods.All... ... Adenosine Aneurysm Cardiac arrest Carotid artery Basilar artery This is a preview of subscription content, log in to check ... Adenosine-induced transient asystole for management of a basilar artery aneurysm. Case report. J Neurosurg. 1999;91:687-90. ... Adenosine-induced transient cardiac arrest may serve as an alternative.. Methods. All patients who underwent microsurgical ...
... seawater or wastewater samples using bioluminescent technology to measure adenosine triphosphate. ...
... -. *Formula: C10H12ClN5O4 ...
The adenosine deaminase (ADA) test is not a diagnostic test, but it may be used along with other tests such as pleural fluid ... Adenosine deaminase (ADA) is a protein that is produced by cells throughout the body and is associated with the activation of ... If adenosine deaminase (ADA) is markedly elevated in pleural fluid in a person with signs and symptoms that suggest ... 2010 October). Adenosine Deaminase Levels in CSF of Tuberculous Meningitis Patients. J Clin Med Res. 2010 October; 2(5): 220- ...
... ,ARUP Laboratories is a national reference laboratory and a worldwide leader in innovative laboratory ...
Learn more about Adenosine uses, effectiveness, possible side effects, interactions, dosage, user ratings and products that ... Adenosine comes in three different forms: adenosine, adenosine monophosphate (AMP), and adenosine triphosphate (ATP).. ... Adenosine Phosphate, Adenosine 5-Triphosphate Disodium, Adenosine; Adenosine Monophosphate (AMP), Adénosine Monophosphate (AMP ... Methylxanthines interacts with ADENOSINE. Methylxanthines might block the affects of adenosine. Adenosine is often used by ...
Twenty years of clinical experience have shown that adenosine is a valuable tool in the management of SVT in infants and ... Administration of adenosine is contraindicated in patients with pre-existing second or third degree heart block or sinus node ... Adenosine for the Management of Neonatal and Pediatric Supraventricular Tachycardia. Contributing Editor: Marcia L. Buck, Pharm ... Adenosine is a respiratory stimulant and may produce severe bronchoconstriction and bronchospasm as a result of mast cell ...
The scientists discovered a new way to stimulate brown fat and thus burn energy from food: The bodys own adenosine activates ... adenosine. Adenosine is typically released during stress. Crucial for transmitting the adenosine signal is the adenosine ... Adenosine activates brown adipose tissue. "If adenosine binds to this receptor in brown fat cells, fat burning is significantly ... "Browning" of white fat by adenosine In addition, the research team investigated the possibility that adenosine transforms white ...
Definition of adenosine 5′-triphosphate. Provided by Stedmans medical dictionary and Drugs.com. Includes medical terms and ... adenosine 5′-triphosphate. Pronunciation: ă-den′ō-sēn trī-fos′fāt. Definition: Adenosine with triphosphoric acid esterified at ... Synonym(s): adenosine triphosphate. Further information. Always consult your healthcare provider to ensure the information ...
  • Adenosine deaminase deficiency (also called ADA deficiency or ADA-SCID) is an autosomal recessive metabolic disorder that causes immunodeficiency. (wikipedia.org)
  • Abstract DESCRIPTION: (Adapted from the Investigator's Abstract): Adenosine administered as an aerosol to asthmatics causes bronchoconstriction, while in non-asthmatics adenosine causes bronchodilation. (sbir.gov)
  • Adenosine deaminases acting on RNA (ADAR) are enzymes responsible for binding to double stranded RNA (dsRNA) and converting adenosine (A) to inosine (I) by deamination. (wikipedia.org)
  • Finally, the researchers determined that this unwinding is due to the deamination of adenosine residues to inosine. (wikipedia.org)
  • scheme of adenosine conversion to inosine via ADAR In humans, the enzyme's active site has 2-3 amino-terminal dsRNA binding domains (dsRBDs) and one carboxy terminal catalytic deaminase domain. (wikipedia.org)
  • Muscle cramping The cause of cramping is unknown, but may be related to elevated lactate, increased calcium signaling across the sarcoplasmic reticulum caused by membrane instability from reduced levels of ATP, or increased levels of free adenosine. (wikipedia.org)
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