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.
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.
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.
A stable adenosine A1 and A2 receptor agonist. Experimentally, it inhibits cAMP and cGMP phosphodiesterase activity.
Purine bases found in body tissues and fluids and in some plants.
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).
N-Isopropyl-N-phenyl-adenosine. Antilipemic agent. Synonym: TH 162.
Compounds that bind to and block the stimulation of PURINERGIC P1 RECEPTORS.
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.
Compounds that bind to and stimulate PURINERGIC P1 RECEPTORS.
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.
A group of compounds that are derivatives of beta- aminoethylbenzene which is structurally and pharmacologically related to amphetamine. (From Merck Index, 11th ed)
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.
An enzyme that catalyzes the hydrolysis of ADENOSINE to INOSINE with the elimination of AMMONIA.
Copolymer of divinyl ether and maleic anhydride that acts as an immunostimulant with antineoplastic and anti-infective properties. It is used in combination with other antineoplastic agents.
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)
Drugs that bind to and block the activation of PURINERGIC RECEPTORS.
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.
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.
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.
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.
A toxic alkaloid found in Amanita muscaria (fly fungus) and other fungi of the Inocybe species. It is the first parasympathomimetic substance ever studied and causes profound parasympathetic activation that may end in convulsions and death. The specific antidote is atropine.
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.

Interruption of transmembrane signaling as a novel antisecretory strategy to treat enterotoxigenic diarrhea. (1/208)

Bacteria that produce heat-stable enterotoxins (STs), a leading cause of secretory diarrhea, are a major cause of morbidity and mortality worldwide. ST stimulates guanylyl cyclase C (GCC) and accumulation of intracellular cyclic GMP ([cGMP]i), which opens the cystic fibrosis transmembrane conductance regulator (CFTR)-related chloride channel, triggering intestinal secretion. Although the signaling cascade mediating ST-induced diarrhea is well characterized, antisecretory therapy targeting this pathway has not been developed. 2-ChloroATP (2ClATP) and its cell-permeant precursor, 2-chloroadenosine (2ClAdo), disrupt ST-dependent signaling in intestinal cells. However, whether the ability to disrupt guanylyl cyclase signaling translates into effective antisecretory therapy remains untested. In this study, the efficacy of 2ClAdo to prevent ST-induced water secretion by human intestinal cells was examined. In Caco-2 human intestinal cells, ST increased [cGMP]i, induced a chloride current, and stimulated net basolateral-to-apical water secretion. This effect on chloride current and water secretion was mimicked by the cell-permeant analog of cGMP, 8-bromo-cGMP. Treatment of Caco-2 cells with 2ClAdo prevented ST-induced increases in [cGMP]i, chloride current and water secretion. Inhibition of the downstream consequences of ST-GCC interaction reflects proximal disruption of cGMP production because 8-bromo-cGMP stimulated chloride current and water secretion in 2ClAdo-treated cells. Thus, this study demonstrates that disruption of guanylyl cyclase signaling is an effective strategy for antisecretory therapy and provides the basis for developing mechanism-based treatments for enterotoxigenic diarrhea.  (+info)

Depletion of alveolar macrophages by treatment with 2-chloroadenosine aerosol. (2/208)

Alveolar macrophages (AMs) are localized in the alveoli and alveolar ducts of the lung and are the only macrophages living in an aerobic environment. Recent studies have demonstrated that AMs play a central role in lung diseases, such as pneumonia and acute respiratory distress syndrome. It has become important to find a simple, effective way to eliminate AMs in order to investigate the function of AMs in vivo. 2-Chloroadenosine (2-CA), a purine analog, is reported to be selectively cytotoxic to cultured macrophages, and we hypothesized that it would deplete the number of AMs in the bronchoalveolar lavage fluid (BALF) of mice without any effect on neutrophil or lymphocyte counts. After mice had inhaled 1 mM aerosolized 2-CA for 2 h, AMs were found to be significantly depleted at 0 h [(4.42 +/- 0.16) x 10(4)/ml], 24 h [(4.17 +/- 0.89) x 10(4)/ml], 48 h [(3.17 +/- 0.21) x 10(4)/ml], and 72 h [(5.00 +/- 0.64) x 10(4)/ml] compared with concentrations in untreated controls [(12.1 +/- 0.21) x 10(4)/ml]. Neutrophil and lymphocyte counts in BALF did not change and histological changes in the lung were not observed after 2-CA treatment. The lung wet-to-dry weight ratio did not change at 0, 24, and 48 h after 2-CA aerosol application. The 2-CA aerosol had no effect on lung vascular permeability, as assessed by the intravenous administration of Evans blue, or on other phagocytes, as assessed by Kupffer cell counts. Our study demonstrates the efficacy of 2-CA in reducing AM numbers in vivo.  (+info)

A(2B) receptors mediate antimitogenesis in vascular smooth muscle cells. (3/208)

Adenosine inhibits growth of vascular smooth muscle cells. The goals of this study were to determine which adenosine receptor subtype mediates the antimitogenic effects of adenosine and to investigate the signal transduction mechanisms involved. In rat aortic vascular smooth muscle cells, platelet-derived growth factor-BB (PDGF-BB) (25 ng/mL) stimulated DNA synthesis ([(3)H]thymidine incorporation), cellular proliferation (cell number), collagen synthesis ([(3)H]proline incorporation), total protein synthesis ([(3)H]leucine incorporation), and mitogen-activated protein (MAP) kinase activity. The adenosine receptor agonists 2-chloroadenosine and 5'-N-methylcarboxamidoadenosine, but not N(6)-cyclopentyladenosine or CGS21680, inhibited the growth effects of PDGF-BB, an agonist profile consistent with an A(2B) receptor-mediated effect. The adenosine receptor antagonists KF17837 and 1,3-dipropyl-8-p-sulfophenylxanthine, but not 8-cyclopentyl-1, 3-dipropylxanthine, blocked the growth-inhibitory effects of 2-chloroadenosine and 5'-N-methylcarboxamidoadenosine, an antagonist profile consistent with an A(2) receptor-mediated effect. Antisense, but not sense or scrambled, oligonucleotides to the A(2B) receptor stimulated basal and PDGF-induced DNA synthesis, cell proliferation, and MAP kinase activity. Moreover, the growth-inhibitory effects of 2-chloroadenosine, 5'-N-methylcarboxamidoadenosine, and erythro-9-(2-hydroxy-3-nonyl) adenine plus iodotubericidin (inhibitors of adenosine deaminase and adenosine kinase, respectively) were abolished by antisense, but not scrambled or sense, oligonucleotides to the A(2B) receptor. Our findings strongly support the hypothesis that adenosine causes inhibition of vascular smooth muscle cell growth by activating A(2B) receptors coupled to inhibition of MAP kinase activity. Pharmacological or molecular biological activation of A(2B) receptors may prevent vascular remodeling associated with hypertension, atherosclerosis, and restenosis following balloon angioplasty.  (+info)

Altered regulation of potassium and calcium channels by GABA(B) and adenosine receptors in hippocampal neurons from mice lacking Galpha(o). (4/208)

To examine the role of G(o) in modulation of ion channels by neurotransmitter receptors, we characterized modulation of ionic currents in hippocampal CA3 neurons from mice lacking both isoforms of Galpha(o). In CA3 neurons from Galpha(o)(-/-) mice, 2-chloro-adenosine and the GABA(B)-receptor agonist baclofen activated inwardly rectifying K(+) currents and inhibited voltage-dependent Ca(2+) currents just as effectively as in Galpha(o)(+/+) littermates. However, the kinetics of transmitter action were dramatically altered in Galpha(o)(-/-) mice in that recovery on washout of agonist was much slower. For example, recovery from 2-chloro-adenosine inhibition of calcium current was more than fourfold slower in neurons from Galpha(o)(-/-) mice [time constant of 12.0 +/- 0.8 (SE) s] than in neurons from Galpha(o)(+/+) mice (time constant of 2.6 +/- 0.2 s). Recovery from baclofen effects was affected similarly. In neurons from control mice, effects of both baclofen and 2-chloro-adenosine on Ca(2+) currents and K(+) currents were abolished by brief exposure to external N-ethyl-maleimide (NEM). In neurons lacking Galpha(o), some inhibition of Ca(2+) currents by baclofen remained after NEM treatment, whereas baclofen activation of K(+) currents and both effects of 2-chloro-adenosine were abolished. These results show that modulation of Ca(2+) and K(+) currents by G protein-coupled receptors in hippocampal neurons does not have an absolute requirement for Galpha(o). However, modulation is changed in the absence of Galpha(o) in having much slower recovery kinetics. A likely possibility is that the very abundant Galpha(o) is normally used but, when absent, can readily be replaced by G proteins with different properties.  (+info)

Possible role of immune surveillance at the initial phase of metastasis produced by B16BL6 melanoma cells. (5/208)

The relationship among the real-time trafficking of lung metastatic B16BL6 cells, metastatic potential, and the injected number of the cells was examined, since the smaller the number of tumor cells injected, the more clearly the immune defense may be observed. When 1x10(6) or 1x10(5) B16BL6 cells were injected into mice via the tail vein, both numbers of cells accumulated in the lung at a similar rate: there was an approximately 10-fold difference in the number of accumulated cells between the two doses. Elimination from the lung was not dependent on the cell number but on the proportion of accumulated cells. However, the injection of 1x10(4) cells resulted in lung accumulation less than one-tenth of that obtained with 1x10(5) cell injection. Metastasis was observed when 1x10(5) or 1x10(6) B16BL6 cells were injected, but not after injection of 1x10(4) cells. To clarify the roles of the immune defense system at the initial phase of metastasis, we challenged macrophage-depleted mice with 1x10(4) tumor cells. Treatment of mice with 2-chloroadenosine prior to the tumor cell challenge cancelled the suppression of not only metastasis but also the lung accumulation. Furthermore, the administration of 2-chloroadenosine following the tumor cell challenge had little effect on the metastatic potential. These results suggest that the immune surveillance whose action was obvious at the low dose of challenged tumor cells functions strongly at the initial phase but not at the advanced stages of the metastatic process, and that macrophages play an important role in the suppression of metastasis.  (+info)

Adenosine A(2A) and A(2B) receptors in cultured human and porcine coronary artery endothelial cells. (6/208)

We investigated the role of the cAMP link to the signal transduction mechanism coupled with adenosine A(2A) and A(2B) receptors in cultured human coronary artery endothelial cells (HCAEC) and porcine coronary artery endothelial cells (PCAEC). 2-[4-[2- inverted question mark2-[(4-aminophenyl)methylcarbonylamino]ethylaminocarbon yl inverted question marketh yl]phenyl]ethylamino-5'- ethylcarboxamidoadenosine ((125)I-PAPA-APEC) (PAPA-APEC) was used to demonstrate the specific binding in PCAEC membranes. The specific binding was saturable and reversible with a maximal number of binding sites (B(max)) of 240 fmol/mg protein, and scatchard analysis revealed a single class of binding site with an equilibrium dissociation constant (K(d)) of 1. 17 +/- 0.035 nM. In competition experiments, adenosine receptor agonists showed the following order of potency (based on IC(50)): 5'-(N-ethylcarboxamido)adenosine (NECA) >/= CGS-21680 > 2-chloroadenosine. This order appears to be consistent with the A(2) adenosine receptor classification. We also studied the effects of adenosine agonists on the accumulation of cAMP as an indirect approach to show the presence of functional A(2) receptors. Similarly, the same adenosine agonists (10(-7)-10(-4) M) elicited the production of cAMP in intact endothelial cells in a dose-dependent manner, exhibiting consistently with the A(2) adenosine receptor classification. A selective A(2A) adenosine receptor antagonist (ZM-241385, 10(-8) M) significantly inhibited the effect of CGS-21680 on cAMP but only partly inhibited the effect of NECA, suggesting the presence of both A(2A) and A(2B) receptors. Western blot analysis further showed the immunoreactivity of A(2A) and A(2B) receptor at 45 and 36 kDa, respectively, in both HCAEC and PCAEC. Direct evidence for the presence of A(2A) and A(2B) receptors in cultured HCAEC and PCAEC by reverse transcription-polymerase chain reaction (RT-PCR), revealed expected PCR product sizes (205 and 173 bp) for A(2A) and A(2B) receptors in HCAEC and PCAEC, respectively. The data show that adenylate cyclase-coupled adenosine A(2A) and A(2B) receptors are present in coronary endothelial cells.  (+info)

Selective transport of adenosine into porcine coronary smooth muscle. (7/208)

Adenosine (ADO), an endogenous regulator of coronary vascular tone, enhances vasorelaxation in the presence of nucleoside transport inhibitors such as dipyridamole. We tested the hypothesis that coronary smooth muscle (CSM) contains a high-affinity transporter for ADO. ADO-mediated relaxation of isolated large and small porcine coronary artery rings was enhanced 12-fold and 3.4-fold, respectively, by the transport inhibitor, S-(4-nitrobenzyl)-6-thioinosine (NBTI). Enhanced relaxation was independent of endothelium and was selective for ADO over synthetic analogs. Uptake of [(3)H]ADO into freshly dissociated CSM cells or endothelium-denuded rings was linear and concentration dependent. Kinetic analysis yielded a maximum uptake (V(max)) of 67 +/- 7.0 pmol. mg protein(-1). min(-1) and a Michaelis constant (K(m)) of 10. 5 +/- 5.8 microM in isolated cells and a V(max) of 5.1 +/- 0.5 pmol. min(-1). mg wet wt(-1) and a K(m) of 17.6 +/- 2.6 microM in intact rings. NBTI inhibited transport into small arteries (IC(50) = 42 nM) and cells. Analyses of extracellular space and diffusion kinetics using [(3)H]sucrose indicate the V(max) and K(m) for ADO transport are sufficient to clear a significant amount of extracellular adenosine. These data indicate CSM possess a high-affinity nucleoside transporter and that the activity of this transporter is sufficient to modulate ADO sensitivity of large and small coronary arteries.  (+info)

A1 adenosine receptors inhibit multiple voltage-gated Ca2+ channel subtypes in acutely isolated rat basolateral amygdala neurons. (8/208)

1. The anticonvulsant properties of 2-chloroadenosine (CADO) in the basolateral amygdala rely on the activation of adenosine-specific heptahelical receptors. We have utilized whole-cell voltage-clamp electrophysiology to examine the modulatory effects of CADO and other adenosine receptor agonists on voltage-gated calcium channels in dissociated basolateral amygdala neurons. 2. CADO, adenosine, and the A1 subtype-selective agonists N6-(L-2-Phenylisopropyl)adenosine (R-PIA) and 2-chloro-N6-cyclopentyladenosine (CCPA) reversibly modulated whole cell Ba2+ currents in a concentration-dependent fashion. CADO inhibition of barium currents was also sensitive to the A1 antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX). 3. The A2A-selective agonist 4-[2-[[6-Amino-9-(N-ethyl-beta-D-ribofuranuronamidosyl)-9H-purin-2-yl]amino]ethyl ]benzenepropanoic acid (CGS21680) was without effect. 4. CADO inhibition was predominantly voltage-dependent and sensitive to the sulphydryl-modifying reagent N:-ethylmaleimide, implicating a membrane-delimited, G(i/o)-coupled signal transduction pathway in the channel regulation. 5. Using Ca2+ channel subtype-selective antagonists, CADO inhibition appeared to target multiple channel subtypes, with the inhibition of omega-conotoxin GVIA-sensitive calcium channels being more prominent. 6. Our results indicate that the anti-convulsant effects CADO in the basolateral amygdala may be mediated, in part, by the A1 receptor-dependent inhibition of voltage gated calcium channels.  (+info)

2-Chloroadenosine is a synthetic, chlorinated analog of adenosine, which is a naturally occurring purine nucleoside. It acts as an antagonist at adenosine receptors and has been studied for its potential effects on the cardiovascular system, including its ability to reduce heart rate and blood pressure. It may also have anti-cancer properties and has been investigated as a potential therapeutic agent in cancer treatment. However, further research is needed to establish its safety and efficacy in clinical settings.

Adenosine is a purine nucleoside that is composed of a sugar (ribose) and the base adenine. It plays several important roles in the body, including serving as a precursor for the synthesis of other molecules such as ATP, NAD+, and RNA.

In the medical context, adenosine is perhaps best known for its use as a pharmaceutical agent to treat certain cardiac arrhythmias. When administered intravenously, it can help restore normal sinus rhythm in patients with paroxysmal supraventricular tachycardia (PSVT) by slowing conduction through the atrioventricular node and interrupting the reentry circuit responsible for the arrhythmia.

Adenosine can also be used as a diagnostic tool to help differentiate between narrow-complex tachycardias of supraventricular origin and those that originate from below the ventricles (such as ventricular tachycardia). This is because adenosine will typically terminate PSVT but not affect the rhythm of VT.

It's worth noting that adenosine has a very short half-life, lasting only a few seconds in the bloodstream. This means that its effects are rapidly reversible and generally well-tolerated, although some patients may experience transient symptoms such as flushing, chest pain, or shortness of breath.

Purinergic receptors are a type of cell surface receptor that bind and respond to purines and pyrimidines, which are nucleotides and nucleosides. These receptors are involved in various physiological processes, including neurotransmission, muscle contraction, and inflammation. There are two main types of purinergic receptors: P1 receptors, which are activated by adenosine, and P2 receptors, which are activated by ATP and other nucleotides.

P2 receptors are further divided into two subtypes: P2X and P2Y. P2X receptors are ionotropic receptors that form cation channels upon activation, allowing the flow of ions such as calcium and sodium into the cell. P2Y receptors, on the other hand, are metabotropic receptors that activate G proteins upon activation, leading to the activation or inhibition of various intracellular signaling pathways.

Purinergic receptors have been found to play a role in many diseases and conditions, including neurological disorders, cardiovascular disease, and cancer. They are also being studied as potential targets for drug development.

Xanthines are a type of natural alkaloids that are found in various plants, including tea leaves, cocoa beans, and mate. The most common xanthines are caffeine, theophylline, and theobromine. These compounds have stimulant effects on the central nervous system and are often used in medication to treat conditions such as asthma, bronchitis, and other respiratory issues.

Caffeine is the most widely consumed xanthine and is found in a variety of beverages like coffee, tea, and energy drinks. It works by blocking adenosine receptors in the brain, which can lead to increased alertness and reduced feelings of fatigue.

Theophylline is another xanthine that is used as a bronchodilator to treat asthma and other respiratory conditions. It works by relaxing smooth muscles in the airways, making it easier to breathe.

Theobromine is found in cocoa beans and is responsible for the stimulant effects of chocolate. While it has similar properties to caffeine and theophylline, it is less potent and has a milder effect on the body.

It's worth noting that while xanthines can have beneficial effects when used in moderation, they can also cause negative side effects such as insomnia, nervousness, and rapid heart rate if consumed in large quantities or over an extended period of time.

Purinergic P1 receptors are a type of G-protein coupled receptor that bind to nucleotides such as adenosine. These receptors are involved in a variety of physiological processes, including modulation of neurotransmitter release, cardiovascular function, and immune response. There are four subtypes of P1 receptors (A1, A2A, A2B, and A3) that have different signaling pathways and functions. Activation of these receptors can lead to a variety of cellular responses, including inhibition or stimulation of adenylyl cyclase activity, changes in intracellular calcium levels, and activation of various protein kinases. They play important roles in the central nervous system, cardiovascular system, respiratory system, gastrointestinal system, and immune system.

Phenylisopropyladenosine (PIA) is not typically defined in the context of medical terminology, but rather it is a term used in pharmacology and biochemistry. PIA is a type of adenosine receptor agonist that specifically binds to and activates the A1 adenosine receptor.

Adenosine receptors are a type of G protein-coupled receptor (GPCR) found in various tissues throughout the body, including the brain, heart, and immune system. Activation of these receptors by agonists like PIA can have diverse effects on cellular function, such as modulating neurotransmission, reducing heart rate and contractility, and regulating inflammation.

While not a medical term per se, PIA is an important compound in the study of adenosine receptor biology and has potential therapeutic applications in various diseases, including neurological disorders, cardiovascular disease, and cancer.

Purinergic P1 receptor antagonists are a class of pharmaceutical drugs that block the activity of purinergic P1 receptors, which are a type of G-protein coupled receptor found in many tissues throughout the body. These receptors are activated by extracellular nucleotides such as adenosine and ATP, and play important roles in regulating a variety of physiological processes, including cardiovascular function, neurotransmission, and immune response.

Purinergic P1 receptor antagonists work by binding to these receptors and preventing them from being activated by nucleotides. This can have various therapeutic effects, depending on the specific receptor subtype that is targeted. For example, A1 receptor antagonists have been shown to improve cardiac function in heart failure, while A2A receptor antagonists have potential as anti-inflammatory and neuroprotective agents.

However, it's important to note that the use of purinergic P1 receptor antagonists is still an area of active research, and more studies are needed to fully understand their mechanisms of action and therapeutic potential.

Theophylline is a medication that belongs to a class of drugs called methylxanthines. It is used in the management of respiratory diseases such as asthma, chronic obstructive pulmonary disease (COPD), and other conditions that cause narrowing of the airways in the lungs.

Theophylline works by relaxing the smooth muscle around the airways, which helps to open them up and make breathing easier. It also acts as a bronchodilator, increasing the flow of air into and out of the lungs. Additionally, theophylline has anti-inflammatory effects that can help reduce swelling in the airways and relieve symptoms such as coughing, wheezing, and shortness of breath.

Theophylline is available in various forms, including tablets, capsules, and liquid solutions. It is important to take this medication exactly as prescribed by a healthcare provider, as the dosage may vary depending on individual factors such as age, weight, and liver function. Regular monitoring of blood levels of theophylline is also necessary to ensure safe and effective use of the medication.

Purinergic P1 receptor agonists are substances that bind to and activate purinergic P1 receptors, which are a type of G protein-coupled receptor found in many tissues throughout the body. These receptors are activated by endogenous nucleotides such as adenosine and its metabolites.

Purinergic P1 receptors include four subtypes: A1, A2A, A2B, and A3. Each of these subtypes has distinct signaling pathways and physiological roles. For example, A1 receptor activation can lead to vasodilation, bradycardia, and anti-inflammatory effects, while A2A receptor activation can increase cyclic AMP levels and have anti-inflammatory effects.

Purinergic P1 receptor agonists are used in various therapeutic applications, including as cardiovascular drugs, antiplatelet agents, and anti-inflammatory agents. Some examples of purinergic P1 receptor agonists include adenosine, regadenoson, and dipyridamole.

It's important to note that the use of these substances should be under medical supervision due to their potential side effects and interactions with other medications.

8-Bromo Cyclic Adenosine Monophosphate (8-Br-cAMP) is a synthetic, cell-permeable analog of cyclic adenosine monophosphate (cAMP). Cyclic AMP is an important second messenger in many signal transduction pathways, and 8-Br-cAMP is often used in research to mimic or study the effects of increased cAMP levels. The bromine atom at the 8-position makes 8-Br-cAMP more resistant to degradation by phosphodiesterases, allowing it to have a longer duration of action compared to cAMP. It is used in various biochemical and cellular studies as a tool compound to investigate the role of cAMP in different signaling pathways.

Phenethylamines are a class of organic compounds that share a common structural feature, which is a phenethyl group (a phenyl ring bonded to an ethylamine chain). In the context of pharmacology and neuroscience, "phenethylamines" often refers to a specific group of psychoactive drugs, including stimulants like amphetamine and mescaline, a classic psychedelic. These compounds exert their effects by modulating the activity of neurotransmitters in the brain, such as dopamine, norepinephrine, and serotonin. It is important to note that many phenethylamines have potential for abuse and are controlled substances.

Adenosine A2B receptor (A2BAR) is a type of G protein-coupled receptor that binds the endogenous purine nucleoside adenosine. It is a subtype of the A2 class of adenosine receptors, which also includes A2A receptor.

The A2BAR is widely expressed in various tissues and cells, including vascular smooth muscle cells, endothelial cells, fibroblasts, immune cells, and epithelial cells. Activation of the A2BAR by adenosine leads to a variety of cellular responses, such as relaxation of vascular smooth muscle, inhibition of platelet aggregation, modulation of inflammatory responses, and stimulation of fibroblast proliferation and collagen production.

The A2BAR has been implicated in several physiological and pathophysiological processes, such as cardiovascular function, pain perception, neuroprotection, tumor growth and metastasis, and pulmonary fibrosis. Therefore, the development of selective A2BAR agonists or antagonists has been an area of active research for therapeutic interventions in these conditions.

Adenosine Deaminase (ADA) is an enzyme that plays a crucial role in the immune system by helping to regulate the levels of certain chemicals called purines within cells. Specifically, ADA helps to break down adenosine, a type of purine, into another compound called inosine. This enzyme is found in all tissues of the body, but it is especially active in the immune system's white blood cells, where it helps to support their growth, development, and function.

ADA deficiency is a rare genetic disorder that can lead to severe combined immunodeficiency (SCID), a condition in which babies are born with little or no functional immune system. This makes them extremely vulnerable to infections, which can be life-threatening. ADA deficiency can be treated with enzyme replacement therapy, bone marrow transplantation, or gene therapy.

Pyran copolymer is not a medical term per se, but it is a chemical compound that has been used in the medical field, particularly in the development of some medications and medical devices.

Pyran copolymer is a synthetic polymer made up of repeating units of furan and maleic anhydride. It is known for its biocompatibility, making it useful in medical applications such as drug delivery systems and implantable devices. The compound has been explored for its potential to reduce the risk of infection and inflammation in these settings.

In summary, pyran copolymer is a synthetic polymer made up of furan and maleic anhydride repeating units, which has been used in medical applications due to its biocompatibility and potential to reduce the risk of infection and inflammation.

Dipyridamole is a medication that belongs to a class of drugs called antiplatelet agents. It works by preventing platelets in your blood from sticking together to form clots. Dipyridamole is often used in combination with aspirin to prevent stroke and other complications in people who have had a heart valve replacement or a type of irregular heartbeat called atrial fibrillation.

Dipyridamole can also be used as a stress agent in myocardial perfusion imaging studies, which are tests used to evaluate blood flow to the heart. When used for this purpose, dipyridamole is given intravenously and works by dilating the blood vessels in the heart, allowing more blood to flow through them and making it easier to detect areas of reduced blood flow.

The most common side effects of dipyridamole include headache, dizziness, and gastrointestinal symptoms such as diarrhea, nausea, and vomiting. In rare cases, dipyridamole can cause more serious side effects, such as allergic reactions, abnormal heart rhythms, or low blood pressure. It is important to take dipyridamole exactly as directed by your healthcare provider and to report any unusual symptoms or side effects promptly.

Purinergic antagonists are a class of drugs that block the action of purinergic receptors, which are specialized proteins found on the surface of cells that respond to purines such as ATP and ADP. These receptors play important roles in various physiological processes, including neurotransmission, inflammation, and cell death.

Purinergic antagonists work by binding to these receptors and preventing them from being activated by purines. This can have a variety of effects depending on the specific receptor that is blocked. For example, some purinergic antagonists are used in the treatment of conditions such as chronic pain, depression, and Parkinson's disease because they block receptors that play a role in these conditions.

It's important to note that while purinergic antagonists can be useful therapeutically, they can also have side effects and potential risks. As with any medication, it's important to use them only under the guidance of a healthcare professional.

Tubercidin is not a medical term itself, but it is a type of antibiotic that belongs to the class of compounds known as nucleoside antibiotics. Specifically, tubercidin is a naturally occurring adenine analogue that is produced by several species of Streptomyces bacteria.

Tubercidin has been found to have antimicrobial and antitumor activities. It works by inhibiting the enzyme adenosine deaminase, which plays a crucial role in the metabolism of nucleotides in cells. By inhibiting this enzyme, tubercidin can interfere with DNA and RNA synthesis, leading to cell death.

While tubercidin has shown promise as an anticancer agent in preclinical studies, its clinical use is limited due to its toxicity and potential for causing mutations in normal cells. Therefore, it is primarily used for research purposes to study the mechanisms of nucleotide metabolism and the effects of nucleoside analogues on cell growth and differentiation.

Adenosine kinase (ADK) is an enzyme that plays a crucial role in the regulation of adenosine levels in cells. The medical definition of adenosine kinase is:

"An enzyme (EC 2.7.1.20) that catalyzes the phosphorylation of adenosine to form adenosine monophosphate (AMP) using ATP as the phosphate donor. This reaction helps maintain the balance between adenosine and its corresponding nucleotides in cells, and it plays a significant role in purine metabolism, cell signaling, and energy homeostasis."

Adenosine kinase is widely distributed in various tissues, including the brain, heart, liver, and muscles. Dysregulation of adenosine kinase activity has been implicated in several pathological conditions, such as ischemia-reperfusion injury, neurodegenerative disorders, and cancer. Therefore, modulating adenosine kinase activity has emerged as a potential therapeutic strategy for treating these diseases.

Cyclic adenosine monophosphate (cAMP) is a key secondary messenger in many biological processes, including the regulation of metabolism, gene expression, and cellular excitability. It is synthesized from adenosine triphosphate (ATP) by the enzyme adenylyl cyclase and is degraded by the enzyme phosphodiesterase.

In the body, cAMP plays a crucial role in mediating the effects of hormones and neurotransmitters on target cells. For example, when a hormone binds to its receptor on the surface of a cell, it can activate a G protein, which in turn activates adenylyl cyclase to produce cAMP. The increased levels of cAMP then activate various effector proteins, such as protein kinases, which go on to regulate various cellular processes.

Overall, the regulation of cAMP levels is critical for maintaining proper cellular function and homeostasis, and abnormalities in cAMP signaling have been implicated in a variety of diseases, including cancer, diabetes, and neurological disorders.

Adenosine A2A receptor is a type of G protein-coupled receptor that binds to the endogenous purine nucleoside, adenosine. It is a subtype of the A2 receptor along with the A2B receptor and is widely distributed throughout the body, particularly in the brain, heart, and immune system.

The A2A receptor plays an essential role in various physiological processes, including modulation of neurotransmission, cardiovascular function, and immune response. In the brain, activation of A2A receptors can have both excitatory and inhibitory effects on neuronal activity, depending on the location and context.

In the heart, A2A receptor activation has a negative chronotropic effect, reducing heart rate, and a negative inotropic effect, decreasing contractility. In the immune system, A2A receptors are involved in regulating inflammation and immune cell function.

Pharmacologically, A2A receptor agonists have been investigated for their potential therapeutic benefits in various conditions, including Parkinson's disease, chronic pain, ischemia-reperfusion injury, and cancer. Conversely, A2A receptor antagonists have also been studied as a potential treatment for neurodegenerative disorders, such as Alzheimer's disease, and addiction.

Muscarine is a naturally occurring organic compound that is classified as an alkaloid. It is found in various mushrooms, particularly those in the Amanita genus such as Amanita muscaria (the fly agaric) and Amanita pantherina. Muscarine acts as a parasympathomimetic, which means it can bind to and stimulate the same receptors as the neurotransmitter acetylcholine in the parasympathetic nervous system. This can lead to various effects on the body, including slowed heart rate, increased salivation, constricted pupils, and difficulty breathing. In high doses, muscarine can be toxic and even life-threatening.

I must clarify that the term "Guinea Pigs" is not typically used in medical definitions. However, in colloquial or informal language, it may refer to people who are used as the first to try out a new medical treatment or drug. This is known as being a "test subject" or "in a clinical trial."

In the field of scientific research, particularly in studies involving animals, guinea pigs are small rodents that are often used as experimental subjects due to their size, cost-effectiveness, and ease of handling. They are not actually pigs from Guinea, despite their name's origins being unclear. However, they do not exactly fit the description of being used in human medical experiments.

Charousová, Ivana; Javoreková, Soňa; Wink, Joachim (2 February 2015). "Isolation and characterization of Streptomyces ... Streptomyces rishiriensis produces coumermycin A1, notomycin, 2-chloroadenosine, phosphophenylalanarginine and lactonamycin. ...
2-chloroadenosine MeSH D13.570.583.138.300.200 - cladribine MeSH D13.570.583.138.325 - deoxyadenosines MeSH D13.570.583.138. ... 2-chloroadenosine MeSH D13.570.800.096.300.200 - cladribine MeSH D13.570.800.096.500 - isopentenyladenosine MeSH D13.570. ...
2-chloroadenosine [Ligand Id: 372] activity data from GtoPdb and ChEMBL. Click here for a description of the charts and data ... ChEMBL ligand: CHEMBL285819 (2-Chloroadenosine) *A1 receptor/Adenosine A1 receptor in Human [ChEMBL: CHEMBL226] [GtoPdb: 18] [ ... Antagonism of cyclic [3H]AMP accumulation elicited by 15 uM 2-chloroadenosine in [3H]adenine-labeled guinea pig cerebral ...
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... chloroadenosine on potassium‐evoked and neurally‐evoked acetylcholine secretion from normal or from latent active zones in the ... chloroadenosine on potassium‐evoked and neurally‐evoked acetylcholine secretion from normal or from latent active zones in the ... Dive into the research topics of The influence of 2‐ ...
5HT-2 ([3H]mianserin; rat forebrain; 0.75 nM; Peroutka & Snyder 1981); 5-HT-1 and 2 ([3H]lysergic acid diethylamide (LSD); 2 nM ... 5-HT-2 and muscarinic cholinergic receptor sites than in inhibiting depolarization dependent calcium fluxes (Donatsch et al ... 2-CADO; 1.0 nM; whole brain crude synaptic membranes; Williams & Risley 1980). Examination of cyproheptadine in eleven receptor ...
Charousová, Ivana; Javoreková, Soňa; Wink, Joachim (2 February 2015). "Isolation and characterization of Streptomyces ... Streptomyces rishiriensis produces coumermycin A1, notomycin, 2-chloroadenosine, phosphophenylalanarginine and lactonamycin. ...
Orally active protease inhibitor; inhibits entry of SARS-Cov-2 into lung cells. ...
Volume: 1 Issue: 2 Year: 2004 Page: 141-147. Author(s): Eva Pongo, Ines Nevelsteen, Erin Liem, Willem Flameng, Kanigula Mubagwa ... Cytostatic Effect of the Nucleoside Analogue 2-Chloroadenosine on Human Prostate Cancer Cell Line. Journal: Current ...
2 In phenylephrine contracted aortic rings concentration-response curves were constructed by cumulative additions (10711 ±1075 ... The contractile response in SHR was abolished by A1 adenosine receptor antagonist N6- endonorbornan-2-yl-9-methyladenine (N- ... 2-p-(-2-carboxyethyl) phenethylamino-5-N-thylcarboxamido adenosine (CGS-21680). 3 A non-speci®c adenosine receptor agonist 2- ... chloroadenosine (CAD) resulted in biphasic response with a small contraction at lower concentrations (1079 ±1078 M) followed ...
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Likewise, monobasic sodium phosphate (20 and 400 mM; 1 ml) and 2-chloroadenosine (50-100 μg) had only trivial effects on the ... Likewise, monobasic sodium phosphate (20 and 400 mM; 1 ml) and 2-chloroadenosine (50-100 μg) had only trivial effects on the ... Likewise, monobasic sodium phosphate (20 and 400 mM; 1 ml) and 2-chloroadenosine (50-100 μg) had only trivial effects on the ... Likewise, monobasic sodium phosphate (20 and 400 mM; 1 ml) and 2-chloroadenosine (50-100 μg) had only trivial effects on the ...
2-Chloroadenosine. A metabolically stable analog of adenosine which acts as an adenosine receptor agonist. The compound has a ... Equilibrative-Nucleoside Transporter 2. A subtype of equilibrative nucleoside transporter proteins that is insensitive to ... DipyridamoleDilazepAdenosineVasodilator AgentsThioinosineThallium RadioisotopesEquilibrative-Nucleoside Transporter 2 ... unlike positron-emission tomography where the positron-electron annihilation results in the emission of 2 photons at 180 ...
Volume: 2 Issue: 3 Year: 2005 Page: 261-267. Author(s): Barney E. Dwyer, Atsushi Takeda, Xiongwei Zhu, George Perry, Mark A. ... Volume: 5 Issue: 2 Year: 2005 Page: 85-102. Author(s): Chung Fai Wong, Alexander Guminski, Nicholas A. Saunders, Andrew J. ... Volume: 1 Issue: 2 Year: 2005 Page: 157-166. Author(s): Yasuhiro Ito ... Cytostatic Effect of the Nucleoside Analogue 2-Chloroadenosine on Human Prostate Cancer Cell Line. Journal: Current ...
Weyand, N. J., Calton, C. M., Higashi, D. L., Kanack, K. J. & So, M., Jan 15 2010, In: Journal of Immunology. 184, 2, p. 694- ... Kondrashov, D. A., Roberts, S. A., Weichsel, A. & Montfort, W. R., Nov 2 2004, In: Biochemistry. 43, 43, p. 13637-13647 11 p.. ... Dietrich, M., Mollenkopf, H., So, M. & Friedrich, A., Jul 2009, In: FEMS Microbiology Letters. 296, 2, p. 248-256 9 p.. ... Harth, G., Haidaris, C. G. & So, M., Mar 1 1989, In: Molecular and Biochemical Parasitology. 33, 2, p. 143-150 8 p.. Research ...
In particular, Fluoroamine is a chemical compound with formula NH2F is seldom studied. We are the first to make use of ...
8-chloroadenosine alters the metabolic profile and downregulates antioxidant and DNA damage repair pathways in macrophages. ... Macer-Wright, J., Sileikaite, I., Rayner, B. & Hawkins, Clare Louise, 2020, In: Chemical Research in Toxicology. 33, 2, p. 402- ...
2-chloroadenosine (CAD) is a non-specific adenosine receptor agonist62 3.6.2. Antagonists¶. *Xanthine *Caffeine (A2A and A1 ... 3.1.2. Effect mediated by A1 receptors¶. 3.1.2.1. Neurophysiological effect in the brain¶. * Inhibition of the release of ... 3.1.2. Effect mediated by A2A receptors¶. 3.1.2.1. Neurophysiological effect in the brain of A2A¶. *Reduction of dopamine D2 ... 4.1.2. Adenosine and adenosine antagonists inhibit D2 receptors in A2A-D2 heteromers¶. A2A-D2 heteromers occur primarily in the ...
2. Gender Differences in the Circadian and Seasonal Variations in Patients with Takotsubo Syndrome: A Multicenter Registry at ... The average postoperative opacification rate in the first case was 7.36 + 1.12 (n = 2) in the RCA, 3.81 + 0.51 (n = 3) in the ... The patency rates of device-dependent SVGs that were 1, 2, 3, 4, 5, 6, 7, and 8 years old were 90.1% ± 1.8%, 87.1% ± 2.3%, 86.1 ... We recently encountered 2 patients with mobile cardiac calcified amorphous tumors who were successfully treated by surgery. ...
2-Chloro-adenosine-induced apoptosis in rat brain neuron-glia primary cultures 1-gen-1995 S. CerutiF. CattabeniG. BurnstockD. ... 2-chloro-adenosine induces a glutamate-dependent calcium response in C2C12 myotubes 1-gen-2000 C. FrankA. GiammarioliL. Falzano ... A novel gliotic P2 receptor mediating cyclooxygenase-2 induction in rat and human astrocytes 1-gen-2000 R. BrambillaS. CerutiW ... 2-Chloro-adenosine-induced apoptosis in rat brain neuron-glia primary cultures. 1995 S. Ceruti, F. Cattabeni, G. Burnstock, D. ...
However, the direct preparation of 8-chloroadenosine and of its mono- and diphosphate derivatives can be achieved by using ... This method may be a convenient way to prepare N6-methyl derivatives of 8-chloroadenosine (78% yield).[‌325‌] ... An analogous chlorination (t-BuOCl, DMF, −70°C, 2 h) of 6-(methylamino)- and 6-(dimethylamino)purine nucleosides gives the ...
For example, coculturing of CD19+ human B cells with CD4+CD25+ alloreactive T cells in the presence of IL-2 and CD28-specific ... 2-chloroadenosine (CADO) was purchased from Sigma-Aldrich and used in place of ADO, because of its greater stability. The ... C) The MFI values for surface expression of the 2 ectonucleotidases are higher in B cells than CD4+ T cells. Data are means ± ... C) The MFI values for surface expression of the 2 ectonucleotidases are higher in B cells than CD4+ T cells. Data are means ± ...
Johnson LF, Williams JG, Abelson HT, Green H, Penman S. Changes in RNA in relation to growth of the fibroblast. III. Posttranscriptional regulation of mRNA formation in resting and growing cells. Cell. 1975 Jan; 4(1):69-75 ...
Cells had been incubated in principal antibody diluted 2-Chloroadenosine (CADO) 1:100 in GSDB for 1 h at area temperature and ... Hence, the mRNA levels of integrin 1, integrin 2, integrin 1, RANKL and ALP mRNA in GroEL-stimulated PDL cells was analyzed ... 0.26 2-Chloroadenosine (CADO) M of every primer, and 2.5 units of Pfu turbo enzyme in 50 l. The mix was warmed at 95C for 2 min ... 2 mM l-glutamine, 50 U/mL penicillin, and 50 mg/mL streptomycin for 16 h. Cells had been then returned on track Ca2+-filled ...
2 -Deoxy-2 -fluoroadenosine 5 -Triphosphate. 10 µmol. 134. 141. 104-02. 2 -Deoxy-2 -fluorocytidine 5 -Triphosphate. 10 µmol. ... 2 -Deoxy-2 -fluoroguanosine 5 -Triphosphate. 10 µmol. 134. 141. 104-04. 2 -Deoxy-2 -fluorouridine 5 -Triphosphate. 10 µmol. 134 ... 2-Deoxy-2-fluoronucleosides & Derivatives. 203-15. 2-Deoxy-2-fluoroguanosine. 1 g. 10 g. 50 g. 105. 906. 4180. 110. 954. ... 2-Deoxy-2-fluoroarabinonucleoside 5-triphosphates Kit, (5 µmol each FANA A,G,C,T or U). 4 x 5 µmol. 697. 734. ...
ELAV-Like Protein 2 D12.776.641.520.500 D12.776.631.520.500 ELAV-Like Protein 3 D12.776.641.520.750 D12.776.631.520.750 ELAV- ... 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine D3.438.79.800 D3.633.100.79.800 2-Aminopurine D3.438.759.138.50 ... quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-hexahydro-3-isobutyl-9,10-dimethoxy- D3.438.834.700 D3.633.100.834.700 4- ... Ataxin-2 D12.776.641.69.750 D12.776.631.69.750 Ataxin-3 D8.811.277.656.300.887.500 D8.811.37.250 D12.776.641.69.875 D12.776. ...
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2-Fluoro-2-deoxyglucose use Fluorodeoxyglucose F18 2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-hexahydro-3-isobutyl-9,10- ... 2-Amino-5-phosphonovaleric Acid use 2-Amino-5-phosphonovalerate 2-Amino-6-(1,2,3-trihydroxypropyl)-4(3H)-pteridinone use ... 2-Oxoisovalerate Dehydrogenase (Lipoamide) use 3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide) 2-PAM Compounds use ... 2-Chloroethyl Alcohol use Ethylene Chlorohydrin 2-Dehydro-3-Deoxyphosphoheptonate Aldolase use 3-Deoxy-7-Phosphoheptulonate ...
2-Fluoro-2-deoxyglucose use Fluorodeoxyglucose F18 2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-hexahydro-3-isobutyl-9,10- ... 2-Amino-5-phosphonovaleric Acid use 2-Amino-5-phosphonovalerate 2-Amino-6-(1,2,3-trihydroxypropyl)-4(3H)-pteridinone use ... 2-Oxoisovalerate Dehydrogenase (Lipoamide) use 3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide) 2-PAM Compounds use ... 2-Chloroethyl Alcohol use Ethylene Chlorohydrin 2-Dehydro-3-Deoxyphosphoheptonate Aldolase use 3-Deoxy-7-Phosphoheptulonate ...

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