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.
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 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.
Compounds that selectively bind to and block the activation of ADENOSINE A2 RECEPTORS.
Compounds that bind to and block the stimulation of PURINERGIC P1 RECEPTORS.
An enzyme that catalyzes the hydrolysis of ADENOSINE to INOSINE with the elimination of AMMONIA.
Compounds that bind to and block the stimulation of ADENOSINE A1 RECEPTORS.
A ligand that binds to but fails to activate the INTERLEUKIN 1 RECEPTOR. It plays an inhibitory role in the regulation of INFLAMMATION and FEVER. Several isoforms of the protein exist due to multiple ALTERNATIVE SPLICING of its mRNA.
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.
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.
Compounds that inhibit or block the activity of NEUROKININ-1 RECEPTORS.
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.
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.
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).
Compounds that selectively bind to and activate ADENOSINE A2 RECEPTORS.
Purine bases found in body tissues and fluids and in some plants.
Compounds that bind to and stimulate ADENOSINE A1 RECEPTORS.
The relationship between the dose of an administered drug and the response of the organism to the drug.
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.
Compounds that bind to and stimulate PURINERGIC P1 RECEPTORS.
Drugs that selectively bind to but do not activate histamine H2 receptors, thereby blocking the actions of histamine. Their clinically most important action is the inhibition of acid secretion in the treatment of gastrointestinal ulcers. Smooth muscle may also be affected. Some drugs in this class have strong effects in the central nervous system, but these actions are not well understood.
A family of hexahydropyridines.
Drugs that bind to but do not activate SEROTONIN 5-HT3 RECEPTORS, thereby blocking the actions of SEROTONIN or SEROTONIN 5-HT3 RECEPTOR AGONISTS.
Drugs that bind to but do not activate excitatory amino acid receptors, thereby blocking the actions of agonists.
Compounds that selectively bind to and block the activation of ADENOSINE A3 RECEPTORS.
Drugs that bind to but do not activate DOPAMINE RECEPTORS, thereby blocking the actions of dopamine or exogenous agonists. Many drugs used in the treatment of psychotic disorders (ANTIPSYCHOTIC AGENTS) are dopamine antagonists, although their therapeutic effects may be due to long-term adjustments of the brain rather than to the acute effects of blocking dopamine receptors. Dopamine antagonists have been used for several other clinical purposes including as ANTIEMETICS, in the treatment of Tourette syndrome, and for hiccup. Dopamine receptor blockade is associated with NEUROLEPTIC MALIGNANT SYNDROME.
Agents that antagonize ANGIOTENSIN RECEPTORS. Many drugs in this class specifically target the ANGIOTENSIN TYPE 1 RECEPTOR.
Drugs that bind to but do not activate SEROTONIN 5-HT2 RECEPTORS, thereby blocking the actions of SEROTONIN or SEROTONIN 5-HT2 RECEPTOR AGONISTS. Included under this heading are antagonists for one or more specific 5-HT2 receptor subtypes.
Chemical substances which inhibit the function of the endocrine glands, the biosynthesis of their secreted hormones, or the action of hormones upon their specific sites.
Compounds that bind to and block the stimulation of PURINERGIC P2 RECEPTORS.
Adenine nucleotide containing one phosphate group esterified to the sugar moiety in the 2'-, 3'-, or 5'-position.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
A stable adenosine A1 and A2 receptor agonist. Experimentally, it inhibits cAMP and cGMP phosphodiesterase activity.
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.
Agents inhibiting the effect of narcotics on the central nervous system.
Drugs that selectively bind to but do not activate histamine H1 receptors, thereby blocking the actions of endogenous histamine. Included here are the classical antihistaminics that antagonize or prevent the action of histamine mainly in immediate hypersensitivity. They act in the bronchi, capillaries, and some other smooth muscles, and are used to prevent or allay motion sickness, seasonal rhinitis, and allergic dermatitis and to induce somnolence. The effects of blocking central nervous system H1 receptors are not as well understood.
Cell surface proteins that bind ENDOTHELINS with high affinity and trigger intracellular changes which influence the behavior of cells.
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.
Drugs that bind to but do not activate MUSCARINIC RECEPTORS, thereby blocking the actions of endogenous ACETYLCHOLINE or exogenous agonists. Muscarinic antagonists have widespread effects including actions on the iris and ciliary muscle of the eye, the heart and blood vessels, secretions of the respiratory tract, GI system, and salivary glands, GI motility, urinary bladder tone, and the central nervous system.
Drugs that bind to but do not activate GABA-A RECEPTORS thereby blocking the actions of endogenous or exogenous GABA-A RECEPTOR AGONISTS.
A group of compounds that are derivatives of beta- aminoethylbenzene which is structurally and pharmacologically related to amphetamine. (From Merck Index, 11th ed)
Drugs that bind to but do not activate histamine receptors, thereby blocking the actions of histamine or histamine agonists. Classical antihistaminics block the histamine H1 receptors only.
Drugs that bind to but do not activate GABA RECEPTORS, thereby blocking the actions of endogenous GAMMA-AMINOBUTYRIC ACID and GABA RECEPTOR AGONISTS.
Drugs that bind to but do not activate serotonin receptors, thereby blocking the actions of serotonin or SEROTONIN RECEPTOR AGONISTS.
A class of drugs designed to prevent leukotriene synthesis or activity by blocking binding at the receptor level.
Glycoproteins which contain sialic acid as one of their carbohydrates. They are often found on or in the cell or tissue membranes and participate in a variety of biological activities.
A subtype of endothelin receptor found predominantly in the VASCULAR SMOOTH MUSCLE. It has a high affinity for ENDOTHELIN-1 and ENDOTHELIN-2.
Cell-surface proteins that bind SEROTONIN and trigger intracellular changes which influence the behavior of cells. Several types of serotonin receptors have been recognized which differ in their pharmacology, molecular biology, and mode of action.
A class of ionotropic glutamate receptors characterized by affinity for N-methyl-D-aspartate. NMDA receptors have an allosteric binding site for glycine which must be occupied for the channel to open efficiently and a site within the channel itself to which magnesium ions bind in a voltage-dependent manner. The positive voltage dependence of channel conductance and the high permeability of the conducting channel to calcium ions (as well as to monovalent cations) are important in excitotoxicity and neuronal plasticity.
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 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.
A potent noncompetitive antagonist of the NMDA receptor (RECEPTORS, N-METHYL-D-ASPARTATE) used mainly as a research tool. The drug has been considered for the wide variety of neurodegenerative conditions or disorders in which NMDA receptors may play an important role. Its use has been primarily limited to animal and tissue experiments because of its psychotropic effects.
Drugs that bind to but do not activate SEROTONIN 5-HT1 RECEPTORS, thereby blocking the actions of SEROTONIN 5-HT1 RECEPTOR AGONISTS. Included under this heading are antagonists for one or more of the specific 5-HT1 receptor subtypes.
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.
Quantitative determination of receptor (binding) proteins in body fluids or tissue using radioactively labeled binding reagents (e.g., antibodies, intracellular receptors, plasma binders).
Drugs that selectively bind to and activate ADENOSINE A3 RECEPTORS.
Cell surface receptors that are specific for INTERLEUKIN-1. Included under this heading are signaling receptors, non-signaling receptors and accessory proteins required for receptor signaling. Signaling from interleukin-1 receptors occurs via interaction with SIGNAL TRANSDUCING ADAPTOR PROTEINS such as MYELOID DIFFERENTIATION FACTOR 88.
Drugs that bind to and block the activation of ADRENERGIC ALPHA-1 RECEPTORS.
Compounds with BENZENE fused to AZEPINES.
N-Isopropyl-N-phenyl-adenosine. Antilipemic agent. Synonym: TH 162.
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.
Drugs that bind to nicotinic cholinergic receptors (RECEPTORS, NICOTINIC) and block the actions of acetylcholine or cholinergic agonists. Nicotinic antagonists block synaptic transmission at autonomic ganglia, the skeletal neuromuscular junction, and at central nervous system nicotinic synapses.
Drugs that bind to and block the activation of PURINERGIC RECEPTORS.
Azoles of two nitrogens at the 1,2 positions, next to each other, in contrast with IMIDAZOLES in which they are at the 1,3 positions.
Compounds with a six membered aromatic ring containing NITROGEN. The saturated version is PIPERIDINES.
Drugs that bind to and block the activation of ADRENERGIC ALPHA-2 RECEPTORS.
Endogenous compounds and drugs that bind to and activate SEROTONIN RECEPTORS. Many serotonin receptor agonists are used as ANTIDEPRESSANTS; ANXIOLYTICS; and in the treatment of MIGRAINE DISORDERS.
Drugs that selectively bind to but do not activate HISTAMINE H3 RECEPTORS. They have been used to correct SLEEP WAKE DISORDERS and MEMORY DISORDERS.
A group of compounds that contain the structure SO2NH2.
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.
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)
Peptides whose amino and carboxy ends are linked together with a peptide bond forming a circular chain. Some of them are ANTI-INFECTIVE AGENTS. Some of them are biosynthesized non-ribosomally (PEPTIDE BIOSYNTHESIS, NON-RIBOSOMAL).
Benzopyrroles with the nitrogen at the number one carbon adjacent to the benzyl portion, in contrast to ISOINDOLES which have the nitrogen away from the six-membered ring.
A biochemical messenger and regulator, synthesized from the essential amino acid L-TRYPTOPHAN. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (RECEPTORS, SEROTONIN) explain the broad physiological actions and distribution of this biochemical mediator.
The interaction of two or more substrates or ligands with the same binding site. The displacement of one by the other is used in quantitative and selective affinity measurements.
Elements of limited time intervals, contributing to particular results or situations.
Compounds that bind to and block the stimulation of PURINERGIC P2X RECEPTORS. Included under this heading are antagonists for specific P2X receptor subtypes.
Seven membered heterocyclic rings containing a NITROGEN atom.
An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.
An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of PAIN, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses.
Drugs that bind to but do not activate GABA-B RECEPTORS thereby blocking the actions of endogenous or exogenous GABA-B RECEPTOR AGONISTS.
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)
The action of a drug that may affect the activity, metabolism, or toxicity of another drug.
Cell surface receptors that bind BRADYKININ and related KININS with high affinity and trigger intracellular changes which influence the behavior of cells. The identified receptor types (B-1 and B-2, or BK-1 and BK-2) recognize endogenous KALLIDIN; t-kinins; and certain bradykinin fragments as well as bradykinin itself.
A 21-amino acid peptide produced in a variety of tissues including endothelial and vascular smooth-muscle cells, neurons and astrocytes in the central nervous system, and endometrial cells. It acts as a modulator of vasomotor tone, cell proliferation, and hormone production. (N Eng J Med 1995;333(6):356-63)
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.
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.
A histamine congener, it competitively inhibits HISTAMINE binding to HISTAMINE H2 RECEPTORS. Cimetidine has a range of pharmacological actions. It inhibits GASTRIC ACID secretion, as well as PEPSIN and GASTRIN output.
A class of cell surface receptors for TACHYKININS with a preference for SUBSTANCE P. Neurokinin-1 (NK-1) receptors have been cloned and are members of the G protein coupled receptor superfamily. They are found on many cell types including central and peripheral neurons, smooth muscle cells, acinar cells, endothelial cells, fibroblasts, and immune cells.
A subtype of endothelin receptor found predominantly in the KIDNEY. It may play a role in reducing systemic ENDOTHELIN levels.
The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM.
The observable response an animal makes to any situation.
A subfamily of G-PROTEIN-COUPLED RECEPTORS that bind the neurotransmitter DOPAMINE and modulate its effects. D2-class receptor genes contain INTRONS, and the receptors inhibit ADENYLYL CYCLASES.
A derivative of benzodiazepine that acts on the cholecystokinin A (CCKA) receptor to antagonize CCK-8's (SINCALIDE) physiological and behavioral effects, such as pancreatic stimulation and inhibition of feeding.
Cell surface proteins that bind cholecystokinin (CCK) with high affinity and trigger intracellular changes influencing the behavior of cells. Cholecystokinin receptors are activated by GASTRIN as well as by CCK-4; CCK-8; and CCK-33. Activation of these receptors evokes secretion of AMYLASE by pancreatic acinar cells, acid and PEPSIN by stomach mucosal cells, and contraction of the PYLORUS and GALLBLADDER. The role of the widespread CCK receptors in the central nervous system is not well understood.
Specific molecular sites or proteins on or in cells to which VASOPRESSINS bind or interact in order to modify the function of the cells. Two types of vasopressin receptor exist, the V1 receptor in the vascular smooth muscle and the V2 receptor in the kidneys. The V1 receptor can be subdivided into V1a and V1b (formerly V3) receptors.
Drugs that bind to but do not activate alpha-adrenergic receptors thereby blocking the actions of endogenous or exogenous adrenergic agonists. Adrenergic alpha-antagonists are used in the treatment of hypertension, vasospasm, peripheral vascular disease, shock, and pheochromocytoma.
A nonapeptide messenger that is enzymatically produced from KALLIDIN in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from MAST CELLS during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter.
The D-enantiomer is a potent and specific antagonist of NMDA glutamate receptors (RECEPTORS, N-METHYL-D-ASPARTATE). The L form is inactive at NMDA receptors but may affect the AP4 (2-amino-4-phosphonobutyrate; APB) excitatory amino acid receptors.
An amine derived by enzymatic decarboxylation of HISTIDINE. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter.
A selective serotonin receptor antagonist with weak adrenergic receptor blocking properties. The drug is effective in lowering blood pressure in essential hypertension. It also inhibits platelet aggregation. It is well tolerated and is particularly effective in older patients.
A subclass of cannabinoid receptor found primarily on central and peripheral NEURONS where it may play a role modulating NEUROTRANSMITTER release.
Drugs that bind to but do not activate SEROTONIN 5-HT4 RECEPTORS, thereby blocking the actions of SEROTONIN or SEROTONIN RECEPTOR AGONISTS.
Drugs that bind to but do not activate ADRENERGIC RECEPTORS. Adrenergic antagonists block the actions of the endogenous adrenergic transmitters EPINEPHRINE and NOREPINEPHRINE.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
Compounds with a BENZENE fused to IMIDAZOLES.
Cell surface proteins that bind THROMBOXANES with high affinity and trigger intracellular changes influencing the behavior of cells. Some thromboxane receptors act via the inositol phosphate and diacylglycerol second messenger systems.
PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.
Injections into the cerebral ventricles.
Derivative of noroxymorphone that is the N-cyclopropylmethyl congener of NALOXONE. It is a narcotic antagonist that is effective orally, longer lasting and more potent than naloxone, and has been proposed for the treatment of heroin addiction. The FDA has approved naltrexone for the treatment of alcohol dependence.
The communication from a NEURON to a target (neuron, muscle, or secretory cell) across a SYNAPSE. In chemical synaptic transmission, the presynaptic neuron releases a NEUROTRANSMITTER that diffuses across the synaptic cleft and binds to specific synaptic receptors, activating them. The activated receptors modulate specific ion channels and/or second-messenger systems in the postsynaptic cell. In electrical synaptic transmission, electrical signals are communicated as an ionic current flow across ELECTRICAL SYNAPSES.
A class of cell surface receptors for tachykinins that prefers neurokinin A; (NKA, substance K, neurokinin alpha, neuromedin L), neuropeptide K; (NPK); or neuropeptide gamma over other tachykinins. Neurokinin-2 (NK-2) receptors have been cloned and are similar to other G-protein coupled receptors.
A specific opiate antagonist that has no agonist activity. It is a competitive antagonist at mu, delta, and kappa opioid 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.
A competitive histamine H2-receptor antagonist. Its main pharmacodynamic effect is the inhibition of gastric secretion.
Compounds that inhibit or block the activity of CANNABINOID RECEPTORS.
An isoquinoline alkaloid obtained from Dicentra cucullaria and other plants. It is a competitive antagonist for GABA-A receptors.
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.
Drugs that bind to and block the activation of ADRENERGIC BETA-2 RECEPTORS.
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.
The rate dynamics in chemical or physical systems.
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.
Use of electric potential or currents to elicit biological responses.
An octapeptide that is a potent but labile vasoconstrictor. It is produced from angiotensin I after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME. The amino acid in position 5 varies in different species. To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II, patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS.
A class of histamine receptors discriminated by their pharmacology and mode of action. Histamine H3 receptors were first recognized as inhibitory autoreceptors on histamine-containing nerve terminals and have since been shown to regulate the release of several neurotransmitters in the central and peripheral nervous systems. (From Biochem Soc Trans 1992 Feb;20(1):122-5)
Drugs that bind to and block the activation of MINERALOCORTICOID RECEPTORS by MINERALOCORTICOIDS such as ALDOSTERONE.
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)
A histamine H1 antagonist. It has mild hypnotic properties and some local anesthetic action and is used for allergies (including skin eruptions) both parenterally and locally. It is a common ingredient of cold remedies.
Cell membrane proteins that bind opioids and trigger intracellular changes which influence the behavior of cells. The endogenous ligands for opioid receptors in mammals include three families of peptides, the enkephalins, endorphins, and dynorphins. The receptor classes include mu, delta, and kappa receptors. Sigma receptors bind several psychoactive substances, including certain opioids, but their endogenous ligands are not known.
An alkylamide found in CAPSICUM that acts at TRPV CATION CHANNELS.
A non-essential amino acid naturally occurring in the L-form. Glutamic acid is the most common excitatory neurotransmitter in the CENTRAL NERVOUS SYSTEM.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
A constitutively expressed subtype of bradykinin receptor that may play a role in the acute phase of the inflammatory and pain response. It has high specificity for intact forms of BRADYKININ and KALLIDIN. The receptor is coupled to G-PROTEIN, GQ-G11 ALPHA FAMILY and G-PROTEIN, GI-GO ALPHA FAMILY signaling proteins.
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.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
An amino acid that, as the D-isomer, is the defining agonist for the NMDA receptor subtype of glutamate receptors (RECEPTORS, NMDA).
Drugs used to cause dilation of the blood vessels.
21-Amino-acid peptides produced by vascular endothelial cells and functioning as potent vasoconstrictors. The endothelin family consists of three members, ENDOTHELIN-1; ENDOTHELIN-2; and ENDOTHELIN-3. All three peptides contain 21 amino acids, but vary in amino acid composition. The three peptides produce vasoconstrictor and pressor responses in various parts of the body. However, the quantitative profiles of the pharmacological activities are considerably different among the three isopeptides.
A subfamily of G-PROTEIN-COUPLED RECEPTORS that bind the neurotransmitter DOPAMINE and modulate its effects. D1-class receptor genes lack INTRONS, and the receptors stimulate ADENYLYL CYCLASES.
Compounds containing 1,3-diazole, a five membered aromatic ring containing two nitrogen atoms separated by one of the carbons. Chemically reduced ones include IMIDAZOLINES and IMIDAZOLIDINES. Distinguish from 1,2-diazole (PYRAZOLES).
Drugs used in the treatment of acute or chronic vascular HYPERTENSION regardless of pharmacological mechanism. Among the antihypertensive agents are DIURETICS; (especially DIURETICS, THIAZIDE); ADRENERGIC BETA-ANTAGONISTS; ADRENERGIC ALPHA-ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; CALCIUM CHANNEL BLOCKERS; GANGLIONIC BLOCKERS; and VASODILATOR AGENTS.
One of the catecholamine NEUROTRANSMITTERS in the brain. It is derived from TYROSINE and is the precursor to NOREPINEPHRINE and EPINEPHRINE. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of receptors (RECEPTORS, DOPAMINE) mediate its action.
The physiological narrowing of BLOOD VESSELS by contraction of the VASCULAR SMOOTH MUSCLE.
Peptides composed of between two and twelve amino acids.
Unstriated and unstriped muscle, one of the muscles of the internal organs, blood vessels, hair follicles, etc. Contractile elements are elongated, usually spindle-shaped cells with centrally located nuclei. Smooth muscle fibers are bound together into sheets or bundles by reticular fibers and frequently elastic nets are also abundant. (From Stedman, 25th ed)
A soluble factor produced by MONOCYTES; MACROPHAGES, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. Interleukin-1 is a general term refers to either of the two distinct proteins, INTERLEUKIN-1ALPHA and INTERLEUKIN-1BETA. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation.
A curved elevation of GRAY MATTER extending the entire length of the floor of the TEMPORAL HORN of the LATERAL VENTRICLE (see also TEMPORAL LOBE). The hippocampus proper, subiculum, and DENTATE GYRUS constitute the hippocampal formation. Sometimes authors include the ENTORHINAL CORTEX in the hippocampal formation.
Cell surface proteins that bind CALCITONIN GENE-RELATED PEPTIDE with high affinity and trigger intracellular changes which influence the behavior of cells. CGRP receptors are present in both the CENTRAL NERVOUS SYSTEM and the periphery. They are formed via the heterodimerization of the CALCITONIN RECEPTOR-LIKE PROTEIN and RECEPTOR ACTIVITY-MODIFYING PROTEIN 1.
A class of opioid receptors recognized by its pharmacological profile. Mu opioid receptors bind, in decreasing order of affinity, endorphins, dynorphins, met-enkephalin, and leu-enkephalin. They have also been shown to be molecular receptors for morphine.
Benzopyrroles with the nitrogen at the number two carbon, in contrast to INDOLES which have the nitrogen adjacent to the six-membered ring.
Cell surface proteins that bind corticotropin-releasing hormone with high affinity and trigger intracellular changes which influence the behavior of cells. The corticotropin releasing-hormone receptors on anterior pituitary cells mediate the stimulation of corticotropin release by hypothalamic corticotropin releasing factor. The physiological consequence of activating corticotropin-releasing hormone receptors on central neurons is not well understood.
Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.
An angiotensin receptor subtype that is expressed at high levels in a variety of adult tissues including the CARDIOVASCULAR SYSTEM, the KIDNEY, the ENDOCRINE SYSTEM and the NERVOUS SYSTEM. Activation of the type 1 angiotensin receptor causes VASOCONSTRICTION and sodium retention.
Compounds capable of relieving pain without the loss of CONSCIOUSNESS.
Cell surface proteins that bind TACHYKININS with high affinity and trigger intracellular changes influencing the behavior of cells. Three classes of tachykinin receptors have been characterized, the NK-1; NK-2; and NK-3; which prefer, respectively, SUBSTANCE P; NEUROKININ A; and NEUROKININ B.
The physical activity of a human or an animal as a behavioral phenomenon.
The largest family of cell surface receptors involved in SIGNAL TRANSDUCTION. They share a common structure and signal through HETEROTRIMERIC G-PROTEINS.
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.
A technique for measuring extracellular concentrations of substances in tissues, usually in vivo, by means of a small probe equipped with a semipermeable membrane. Substances may also be introduced into the extracellular space through the membrane.
Cell surface proteins that bind ANGIOTENSINS and trigger intracellular changes influencing the behavior of cells.
Cell surface receptors that bind signalling molecules released by neurons and convert these signals into intracellular changes influencing the behavior of cells. Neurotransmitter is used here in its most general sense, including not only messengers that act to regulate ion channels, but also those which act on second messenger systems and those which may act at a distance from their release sites. Included are receptors for neuromodulators, neuroregulators, neuromediators, and neurohumors, whether or not located at synapses.
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.
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 activate dopamine receptors.
A class of drugs that act by selective inhibition of calcium influx through cellular membranes.
The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.
A competitive serotonin type 3 receptor antagonist. It is effective in the treatment of nausea and vomiting caused by cytotoxic chemotherapy drugs, including cisplatin, and has reported anxiolytic and neuroleptic properties.
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.
A class of opioid receptors recognized by its pharmacological profile. Kappa opioid receptors bind dynorphins with a higher affinity than endorphins which are themselves preferred to enkephalins.
The physiological widening of BLOOD VESSELS by relaxing the underlying VASCULAR SMOOTH MUSCLE.
The principal alkaloid in opium and the prototype opiate analgesic and narcotic. Morphine has widespread effects in the central nervous system and on smooth muscle.
Two-ring crystalline hydrocarbons isolated from coal tar. They are used as intermediates in chemical synthesis, as insect repellents, fungicides, lubricants, preservatives, and, formerly, as topical antiseptics.
The most common inhibitory neurotransmitter in the central nervous system.
A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.
A drug that exerts an inhibitory effect on gastric secretion and reduces gastrointestinal motility. It is used clinically in the drug therapy of gastrointestinal ulcers.
1,4-Diethylene dioxides. Industrial solvents. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), dioxane itself may "reasonably be anticipated to be a carcinogen." (Merck Index, 11th ed)
A serotonin receptor subtype found widely distributed in peripheral tissues where it mediates the contractile responses of variety of tissues that contain SMOOTH MUSCLE. Selective 5-HT2A receptor antagonists include KETANSERIN. The 5-HT2A subtype is also located in BASAL GANGLIA and CEREBRAL CORTEX of the BRAIN where it mediates the effects of HALLUCINOGENS such as LSD.
A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.
A process leading to shortening and/or development of tension in muscle tissue. Muscle contraction occurs by a sliding filament mechanism whereby actin filaments slide inward among the myosin filaments.
A phenyl-piperidinyl-butyrophenone that is used primarily to treat SCHIZOPHRENIA and other PSYCHOSES. It is also used in schizoaffective disorder, DELUSIONAL DISORDERS, ballism, and TOURETTE SYNDROME (a drug of choice) and occasionally as adjunctive therapy in INTELLECTUAL DISABILITY and the chorea of HUNTINGTON DISEASE. It is a potent antiemetic and is used in the treatment of intractable HICCUPS. (From AMA Drug Evaluations Annual, 1994, p279)
The study of the generation and behavior of electrical charges in living organisms particularly the nervous system and the effects of electricity on living organisms.
AMANTADINE derivative that has some dopaminergic effects. It has been proposed as an antiparkinson agent.
The number of times the HEART VENTRICLES contract per unit of time, usually per minute.
A class of histamine receptors discriminated by their pharmacology and mode of action. Histamine H2 receptors act via G-proteins to stimulate ADENYLYL CYCLASES. Among the many responses mediated by these receptors are gastric acid secretion, smooth muscle relaxation, inotropic and chronotropic effects on heart muscle, and inhibition of lymphocyte function. (From Biochem Soc Trans 1992 Feb;20(1):122-5)
The injection of very small amounts of fluid, often with the aid of a microscope and microsyringes.
A serotonin receptor (5HT-3 selective) antagonist that has been used as an antiemetic for cancer chemotherapy patients.
Catalyze the hydrolysis of nucleosides with the elimination of ammonia.
An electrophysiologic technique for studying cells, cell membranes, and occasionally isolated organelles. All patch-clamp methods rely on a very high-resistance seal between a micropipette and a membrane; the seal is usually attained by gentle suction. The four most common variants include on-cell patch, inside-out patch, outside-out patch, and whole-cell clamp. Patch-clamp methods are commonly used to voltage clamp, that is control the voltage across the membrane and measure current flow, but current-clamp methods, in which the current is controlled and the voltage is measured, are also used.
Compounds that bind to and block the stimulation of PURINERGIC P2Y RECEPTORS. Included under this heading are antagonists for specific P2Y receptor subtypes.
Established cell cultures that have the potential to propagate indefinitely.

Contribution of adenosine to the depression of sympathetically evoked vasoconstriction induced by systemic hypoxia in the rat. (1/257)

Previous studies have shown that systemic hypoxia evokes vasodilatation in skeletal muscle that is mediated mainly by adenosine acting on A1 receptors, and that the vasoconstrictor effects of sympathetic nerve activity are depressed during hypoxia. The aim of the present study was to investigate the role of adenosine in this depression. In anaesthetised rats, increases in femoral vascular resistance (FVR) evoked by stimulation of the lumbar sympathetic chain with bursts of impulses at 40 or 20 Hz were greater than those evoked by continuous stimulation at 2 Hz with the same number of impulses (120) over 1 min. All of these responses were substantially reduced by infusion of adenosine or by graded systemic hypoxia (breathing 12, 10 or 8 % O2), increases in FVR evoked by continuous stimulation at 2 Hz being most vulnerable. Blockade of A1 receptors ameliorated the depression caused by adenosine infusion of the increase in FVR evoked by 2 Hz only and did not ameliorate the depression caused by 8 % O2 of increases in FVR evoked by any pattern of sympathetic stimulation. A2A receptor blockade accentuated hypoxia-induced depression of the increase in FVR evoked by burst stimulation at 40 Hz, but had no other effect. Neither A1 nor A2A receptor blockade affected the depression caused by hypoxia (8 % O2) of the FVR increase evoked by noradrenaline infusion. These results indicate that endogenously released adenosine is not responsible for the depression of sympathetically evoked muscle vasoconstriction caused by systemic hypoxia; adenosine may exert a presynaptic facilitatory influence on the vasoconstrictor responses evoked by bursts at high frequency.  (+info)

Neuroprotection by caffeine and adenosine A2A receptor blockade of beta-amyloid neurotoxicity. (2/257)

Adenosine is a neuromodulator in the nervous system and it has recently been observed that pharmacological blockade or gene disruption of adenosine A(2A) receptors confers neuroprotection under different neurotoxic situations in the brain. We now observed that coapplication of either caffeine (1-25 micro M) or the selective A(2A) receptor antagonist, 4-(2-[7-amino-2(2-furyl)(1,2,4)triazolo (2,3-a)(1,3,5)triazin-5-ylamino]ethyl)phenol (ZM 241385, 50 nM), but not the A receptor antagonist, 8-cyclopentyltheophylline (200 nM), prevented the neuronal cell death caused by exposure of rat cultured cerebellar granule neurons to fragment 25-35 of beta-amyloid protein (25 micro M for 48 h), that by itself caused a near three-fold increase of propidium iodide-labeled cells. This constitutes the first in vitro evidence to suggest that adenosine A(2A) receptors may be the molecular target responsible for the observed beneficial effects of caffeine consumption in the development of Alzheimer's disease.  (+info)

Synergistic effect of SCH 58261, an adenosine A2A receptor antagonist, and L-DOPA on the reserpine-induced muscle rigidity in rats. (3/257)

The aim of the present study was to find out whether a blockade of adenosine A2A receptors by the selective antagonist, SCH 58261, potentiates the attenuating effect of L-DOPA, the well-known antiparkinsonian drug, on parkinsonian-like muscle rigidity in rats. Muscle tone was examined using a combined mechano- and electromyographic method, which simultaneously measured muscle resistance of a rat hindfoot to passive extension and flexion in the ankle joint and the electromyographic (EMG) activity of the antagonistic muscles of that joint: gastrocnemius and tibialis anterior. Muscle rigidity was produced by reserpine (5 mg/kg ip) injected in combination with alpha-methyl-p-tyrosine (alpha-MT, 250 mg/kg ip). L-DOPA (25 mg/kg ip) or SCH 58261 (0.1 mg/kg ip) administered separately, slightly influenced the reserpine + alpha-MT-induced muscle rigidity. However, only ankle joint extension was affected significantly while the effect on flexion of the rat hindfoot was not significant. Neither L-DOPA nor SCH 58261 given separately modified the reserpine-enhanced tonic or reflex EMG activities in both muscles examined. However, when L-DOPA (25 mg/kg) was given together with SCH 58261 (0.1 mg/kg), a clear synergistic effect was seen on both examined movements and muscles. The present results show that the blockade of adenosine A2A receptors potentiates the antiparkinsonian effect of L-DOPA. Since such an effect was seen in different animal models of Parkinson's disease (PD), it seems that co-administration of SCH 58261 may allow for the lowering of the doses of L-DOPA in clinical practice, which indicates a potential therapeutic value of this compound in the treatment of PD.  (+info)

Brief, repeated, oxygen-glucose deprivation episodes protect neurotransmission from a longer ischemic episode in the in vitro hippocampus: role of adenosine receptors. (4/257)

1. Ischemic preconditioning in the brain consists of reducing the sensitivity of neuronal tissue to further, more severe, ischemic insults. We recorded field epsps (fepsps) extracellularly from hippocampal slices to develop a model of in vitro ischemic preconditioning and to evaluate the role of A1, A2A and A3 adenosine receptors in this phenomenon. 2. The application of an ischemic insult, obtained by glucose and oxygen deprivation for 7 min, produced an irreversible depression of synaptic transmission. Ischemic preconditioning was induced by four ischemic insults (2 min each) separated by 13 min of normoxic conditions. After 30 min, an ischemic insult of 7 min was applied. This protocol substantially protected the tissue from the irreversible depression of synaptic activity. 3. The selective adenosine A1 receptor antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 100 nm), completely prevented the protective effect of preconditioning. The selective adenosine A2A receptor antagonist 4-(2-[7-amino-2-(2-furyl)[1,2,4]triazolo[2,3-a][1,3,5]triazin-5-ylamino]ethyl)phe nol (ZM 241385, 100 nm) did not modify the magnitude of fepsp recovery compared to control slices. The selective A3 adenosine receptor antagonists, 3-propyl-6-ethyl-5[ethyl(thio)carbonyl]-2-phenyl-4-propyl-3-pyridinecarboxylate (MRS 1523, 100 nm) significantly improved the recovery of fepsps after 7 min of ischemia. 4. Our results show that in vitro ischemic preconditioning allows CA1 hippocampal neurons to become resistant to prolonged exposure to ischemia. Adenosine, by stimulating A1 receptors, plays a crucial role in eliciting the cell mechanisms underlying preconditioning; A2A receptors are not involved in this phenomenon, whereas A3 receptor activation is harmful to ischemic preconditioning.  (+info)

Adenosine-induced IL-6 expression in pituitary folliculostellate cells is mediated via A2b adenosine receptors coupled to PKC and p38 MAPK. (5/257)

Activation of adenosine receptors in folliculostellate (FS) cells of the pituitary gland leads to the secretion of IL-6 and vascular endothelial growth factor (VEGF). We investigated the action of adenosine A2 receptor agonists on IL-6 and VEGF secretion in two murine FS cell lines (TtT/GF and Tpit/F1), and demonstrated a rank order of potency, 5'-N-ethylcarboxamidoadenosine (NECA)>2-p-(2-carboxyethyl)phenethylamino-5'-N-ethylcarboxamidoadenosine>adenosin e, suggesting mediation via the A2b receptor. NECA-mediated IL-6 release was inhibited by the PLC inhibitor 1-[6-((17beta-3-methoxyestra-1,3,5(10)-tiene-17-yl)amino)hexyl]-1H-pyrrole-2,5-di one, the PI3 kinase inhibitor wortmannin and the PKC inhibitors bisindolylmaleimide 1 and bisindolymaleimide X1 HCl (Ro-32-0432). NECA-mediated IL-6 release was attenuated (<50%) by the extracellular signal-regulated kinase MAPK inhibitor 2'-amino-3'-methoxyflavone, and completely (>95%) inhibited by the p38 MAPK inhibitor 4-(4-fluorophenyl)-2-(4-methylsulphinylphenyl)-5-(4-pyridyl)1H-imidazole. NECA stimulates p38 MAPK phosphorylation that is inhibited by Ro-32-0432 but not by wortmannin. Dexamethasone inhibits NECA-stimulated IL-6 and VEGF secretion. These findings indicate that adenosine can stimulate IL-6 secretion in FS cells via the A2b receptor coupled principally to PLC/PKC and p38 MAPK; such an action may be important in the modulation of inflammatory response processes in the pituitary gland.  (+info)

Possible targeting of G protein coupled receptors to manipulate inflammation in vivo using synthetic and natural ligands. (6/257)

Cyclic AMP elevating Gs protein coupled receptors were considered for a long time to be immunosuppressive. One of these receptors, adenosine A(2A) receptor, was implicated in a physiological mechanism that down regulates inflammation and protects tissues from excessive immune mediated damage. Targeting of these receptors by selective agonists may lead to better protocols of anti-inflammatory treatments. At the same time inhibiting the Gs protein coupled mediated signalling with antagonists could be explored in studies of approaches to enhance inflammation and tissue damage. Enhancement of targeted tissue damage is highly desirable when it is cancerous tissue, while enhancement of inflammatory events might be desirable in the development of new vaccine adjuvants.  (+info)

Involvement of adenosine A1 and A2A receptors in the adenosinergic modulation of the discriminative-stimulus effects of cocaine and methamphetamine in rats. (7/257)

Adenosine, by acting on adenosine A1 and A2A receptors, is known to antagonistically modulate dopaminergic neurotransmission. We have recently reported that nonselective adenosine receptor antagonists (caffeine and 3,7-dimethyl-1-propargylxanthine) can partially substitute for the discriminative-stimulus effects of methamphetamine. In the present study, by using more selective compounds, we investigated the involvement of A1 and A2A receptors in the adenosinergic modulation of the discriminative-stimulus effects of both cocaine and methamphetamine. The effects of the A1 receptor agonist N6-cyclopentyladenosine (CPA; 0.01-0.1 mg/kg) and antagonist 8-cyclopentyl-1,3-dimethylxanthine (CPT; 1.3-23.7 mg/kg) and the A2A receptor agonist 2-p-(2-carboxyethyl)phenethylamino-5'-N-ethylcarboxamidoadenosine hydrochloride (CGS 21680; 0.03-0.18 mg/kg) and antagonist 3-(3-hydroxypropyl)-8-(3-methoxystyryl)-7-methyl-1-propargylxanthin phosphate disodium salt (MSX-3; 1-56 mg/kg) were evaluated in rats trained to discriminate either 1 mg/kg methamphetamine or 10 mg/kg cocaine from saline under a fixed-ratio 10 schedule of food presentation. The A1 and A2A receptor antagonists (CPT and MSX-3) both produced high levels of drug-lever selection when substituted for either methamphetamine or cocaine and significantly shifted dose-response curves of both psychostimulants to the left. Unexpectedly, the A2A receptor agonist CGS 21680 also produced drug-appropriate responding (although at lower levels) when substituted for the cocaine-training stimulus, and both CGS 21680 and the A1 receptor agonist CPA significantly shifted the cocaine dose-response curve to the left. In contrast, both agonists did not produce significant levels of drug-lever selection when substituted for the methamphetamine-training stimulus and failed to shift the methamphetamine dose-response curve. Therefore, adenosine A1 and A2A receptors appear to play important but differential roles in the modulation of the discriminative-stimulus effects of methamphetamine and cocaine.  (+info)

Antinociceptive effects of novel A2B adenosine receptor antagonists. (8/257)

Caffeine, an adenosine A1, A2A, and A2B receptor antagonist, is frequently used as an adjuvant analgesic in combination with nonsteroidal anti-inflammatory drugs or opioids. In this study, we have examined the effects of novel specific adenosine receptor antagonists in an acute animal model of nociception. Several A2B-selective compounds showed antinociceptive effects in the hot-plate test. In contrast, A1- and A2A-selective compounds did not alter pain thresholds, and an A3 adenosine receptor antagonist produced thermal hyperalgesia. Evaluation of psychostimulant effects of these compounds in the open field showed only small effects of some antagonists at high doses. Coadministration of low, subeffective doses of A2B-selective antagonists with a low dose of morphine enhanced the efficacy of morphine. Our results indicate that analgesic effects of caffeine are mediated, at least in part, by A2B adenosine receptors.  (+info)

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

Hyperalgesia is often seen in people with chronic pain conditions, such as fibromyalgia, and it can also be a side effect of certain medications or medical procedures. Treatment options for hyperalgesia depend on the underlying cause of the condition, but may include pain management techniques, physical therapy, and medication adjustments.

In clinical settings, hyperalgesia is often assessed using a pinprick test or other pain tolerance tests to determine the patient's sensitivity to different types of stimuli. The goal of treatment is to reduce the patient's pain and improve their quality of life.

There are several different types of pain, including:

1. Acute pain: This type of pain is sudden and severe, and it usually lasts for a short period of time. It can be caused by injuries, surgery, or other forms of tissue damage.
2. Chronic pain: This type of pain persists over a long period of time, often lasting more than 3 months. It can be caused by conditions such as arthritis, fibromyalgia, or nerve damage.
3. Neuropathic pain: This type of pain results from damage to the nervous system, and it can be characterized by burning, shooting, or stabbing sensations.
4. Visceral pain: This type of pain originates in the internal organs, and it can be difficult to localize.
5. Psychogenic pain: This type of pain is caused by psychological factors such as stress, anxiety, or depression.

The medical field uses a range of methods to assess and manage pain, including:

1. Pain rating scales: These are numerical scales that patients use to rate the intensity of their pain.
2. Pain diaries: These are records that patients keep to track their pain over time.
3. Clinical interviews: Healthcare providers use these to gather information about the patient's pain experience and other relevant symptoms.
4. Physical examination: This can help healthcare providers identify any underlying causes of pain, such as injuries or inflammation.
5. Imaging studies: These can be used to visualize the body and identify any structural abnormalities that may be contributing to the patient's pain.
6. Medications: There are a wide range of medications available to treat pain, including analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), and muscle relaxants.
7. Alternative therapies: These can include acupuncture, massage, and physical therapy.
8. Interventional procedures: These are minimally invasive procedures that can be used to treat pain, such as nerve blocks and spinal cord stimulation.

It is important for healthcare providers to approach pain management with a multi-modal approach, using a combination of these methods to address the physical, emotional, and social aspects of pain. By doing so, they can help improve the patient's quality of life and reduce their suffering.

Vomiting can be caused by a variety of factors, such as:

1. Infection: Viral or bacterial infections can inflame the stomach and intestines, leading to vomiting.
2. Food poisoning: Consuming contaminated or spoiled food can cause vomiting.
3. Motion sickness: Traveling by car, boat, plane, or other modes of transportation can cause motion sickness, which leads to vomiting.
4. Alcohol or drug overconsumption: Drinking too much alcohol or taking certain medications can irritate the stomach and cause vomiting.
5. Pregnancy: Hormonal changes during pregnancy can cause nausea and vomiting, especially during the first trimester.
6. Other conditions: Vomiting can also be a symptom of other medical conditions such as appendicitis, pancreatitis, and migraines.

When someone is vomiting, they may experience:

1. Nausea: A feeling of queasiness or sickness in the stomach.
2. Abdominal pain: Crampy or sharp pain in the abdomen.
3. Diarrhea: Loose, watery stools.
4. Dehydration: Loss of fluids and electrolytes.
5. Headache: A throbbing headache can occur due to dehydration.
6. Fatigue: Weakness and exhaustion.

Treatment for vomiting depends on the underlying cause, but may include:

1. Fluid replacement: Drinking fluids to replenish lost electrolytes and prevent dehydration.
2. Medications: Anti-inflammatory drugs or antibiotics may be prescribed to treat infections or other conditions causing vomiting.
3. Rest: Resting the body and avoiding strenuous activities.
4. Dietary changes: Avoiding certain foods or substances that trigger vomiting.
5. Hospitalization: In severe cases of vomiting, hospitalization may be necessary to monitor and treat underlying conditions.

It is important to seek medical attention if the following symptoms occur with vomiting:

1. Severe abdominal pain.
2. Fever above 101.5°F (38.6°C).
3. Blood in vomit or stools.
4. Signs of dehydration, such as excessive thirst, dark urine, or dizziness.
5. Vomiting that lasts for more than 2 days.
6. Frequent vomiting with no relief.

It is important to note that catalepsy is not the same as catatonia, which is a more specific condition characterized by a wide range of symptoms, including immobility, mutism, negativism, and emotional dysregulation. However, catalepsy and catatonia do share some similarities, and the terms are often used interchangeably in clinical practice.

The exact cause of catalepsy is not fully understood, but it is thought to be related to dysfunction in certain areas of the brain, such as the neocortex and basal ganglia. In some cases, catalepsy may be a side effect of medication or drug intoxication.

Treatment for catalepsy typically focuses on addressing the underlying cause, such as managing seizures or withdrawing from drugs. In some cases, medications such as benzodiazepines or antipsychotics may be used to help manage symptoms. Other approaches, such as physical therapy and behavioral interventions, may also be helpful in improving mobility and function.

There are several key features of inflammation:

1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.

Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.

There are several types of inflammation, including:

1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.

There are several ways to reduce inflammation, including:

1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.

It's important to note that chronic inflammation can lead to a range of health problems, including:

1. Arthritis
2. Diabetes
3. Heart disease
4. Cancer
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.

Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.

There are several types of edema, including:

1. Pitting edema: This type of edema occurs when the fluid accumulates in the tissues and leaves a pit or depression when it is pressed. It is commonly seen in the skin of the lower legs and feet.
2. Non-pitting edema: This type of edema does not leave a pit or depression when pressed. It is often seen in the face, hands, and arms.
3. Cytedema: This type of edema is caused by an accumulation of fluid in the tissues of the limbs, particularly in the hands and feet.
4. Edema nervorum: This type of edema affects the nerves and can cause pain, numbness, and tingling in the affected area.
5. Lymphedema: This is a condition where the lymphatic system is unable to properly drain fluid from the body, leading to swelling in the arms or legs.

Edema can be diagnosed through physical examination, medical history, and diagnostic tests such as imaging studies and blood tests. Treatment options for edema depend on the underlying cause, but may include medications, lifestyle changes, and compression garments. In some cases, surgery or other interventions may be necessary to remove excess fluid or tissue.

There are different types of anoxia, including:

1. Cerebral anoxia: This occurs when the brain does not receive enough oxygen, leading to cognitive impairment, confusion, and loss of consciousness.
2. Pulmonary anoxia: This occurs when the lungs do not receive enough oxygen, leading to shortness of breath, coughing, and chest pain.
3. Cardiac anoxia: This occurs when the heart does not receive enough oxygen, leading to cardiac arrest and potentially death.
4. Global anoxia: This is a complete lack of oxygen to the entire body, leading to widespread tissue damage and death.

Treatment for anoxia depends on the underlying cause and the severity of the condition. In some cases, hospitalization may be necessary to provide oxygen therapy, pain management, and other supportive care. In severe cases, anoxia can lead to long-term disability or death.

Prevention of anoxia is important, and this includes managing underlying medical conditions such as heart disease, diabetes, and respiratory problems. It also involves avoiding activities that can lead to oxygen deprivation, such as scuba diving or high-altitude climbing, without proper training and equipment.

In summary, anoxia is a serious medical condition that occurs when there is a lack of oxygen in the body or specific tissues or organs. It can cause cell death and tissue damage, leading to serious health complications and even death if left untreated. Early diagnosis and treatment are crucial to prevent long-term disability or death.

* Anxiety
* Depression
* Fatigue
* Insomnia
* Muscle and bone pain
* Nausea and vomiting
* Seizures (in severe cases)
* Sweating
* Tremors

The specific symptoms of substance withdrawal syndrome can vary depending on the substance being withdrawn from, but some common symptoms include:

* Alcohol: tremors, anxiety, insomnia, nausea and vomiting, headaches, and seizures
* Opioids: withdrawal symptoms can include anxiety, muscle aches, sweating, nausea and vomiting, diarrhea, and depression
* Benzodiazepines: withdrawal symptoms can include anxiety, insomnia, tremors, and seizures

The diagnosis of substance withdrawal syndrome is typically made based on the patient's history of substance use and the presence of withdrawal symptoms. A healthcare provider may also order laboratory tests to rule out other conditions that may be causing the symptoms. Treatment for substance withdrawal syndrome usually involves supportive care, such as rest, hydration, and pain management, as well as medication to manage withdrawal symptoms. In some cases, medical professionals may also recommend a gradual tapering of the substance over a period of time to minimize withdrawal symptoms.

It is important for individuals who are experiencing withdrawal symptoms to seek medical attention as soon as possible, as untreated withdrawal can lead to serious complications, such as seizures and dehydration. With appropriate treatment, most individuals with substance withdrawal syndrome can recover fully and successfully overcome their addiction.

In some cases, hyperemia can be a sign of a more serious underlying condition that requires medical attention. For example, if hyperemia is caused by an inflammatory or infectious process, it may lead to tissue damage or organ dysfunction if left untreated.

Hyperemia can occur in various parts of the body, including the skin, muscles, organs, and other tissues. It is often diagnosed through physical examination and imaging tests such as ultrasound, computed tomography (CT), or magnetic resonance imaging (MRI). Treatment for hyperemia depends on its underlying cause, and may include antibiotics, anti-inflammatory medications, or surgery.

In the context of dermatology, hyperemia is often used to describe a condition called erythema, which is characterized by redness and swelling of the skin due to increased blood flow. Erythema can be caused by various factors, such as sun exposure, allergic reactions, or skin infections. Treatment for erythema may include topical medications, oral medications, or other therapies depending on its underlying cause.

There are many different types of seizures, each with its own unique set of symptoms. Some common types of seizures include:

1. Generalized seizures: These seizures affect both sides of the brain and can cause a range of symptoms, including convulsions, loss of consciousness, and muscle stiffness.
2. Focal seizures: These seizures affect only one part of the brain and can cause more specific symptoms, such as weakness or numbness in a limb, or changes in sensation or vision.
3. Tonic-clonic seizures: These seizures are also known as grand mal seizures and can cause convulsions, loss of consciousness, and muscle stiffness.
4. Absence seizures: These seizures are also known as petit mal seizures and can cause a brief loss of consciousness or staring spell.
5. Myoclonic seizures: These seizures can cause sudden, brief muscle jerks or twitches.
6. Atonic seizures: These seizures can cause a sudden loss of muscle tone, which can lead to falls or drops.
7. Lennox-Gastaut syndrome: This is a rare and severe form of epilepsy that can cause multiple types of seizures, including tonic, atonic, and myoclonic seizures.

Seizures can be diagnosed through a combination of medical history, physical examination, and diagnostic tests such as electroencephalography (EEG) or imaging studies. Treatment for seizures usually involves anticonvulsant medications, but in some cases, surgery or other interventions may be necessary.

Overall, seizures are a complex and multifaceted symptom that can have a significant impact on an individual's quality of life. It is important to seek medical attention if you or someone you know is experiencing seizures, as early diagnosis and treatment can help to improve outcomes and reduce the risk of complications.

There are two types of hypertension:

1. Primary Hypertension: This type of hypertension has no identifiable cause and is also known as essential hypertension. It accounts for about 90% of all cases of hypertension.
2. Secondary Hypertension: This type of hypertension is caused by an underlying medical condition or medication. It accounts for about 10% of all cases of hypertension.

Some common causes of secondary hypertension include:

* Kidney disease
* Adrenal gland disorders
* Hormonal imbalances
* Certain medications
* Sleep apnea
* Cocaine use

There are also several risk factors for hypertension, including:

* Age (the risk increases with age)
* Family history of hypertension
* Obesity
* Lack of exercise
* High sodium intake
* Low potassium intake
* Stress

Hypertension is often asymptomatic, and it can cause damage to the blood vessels and organs over time. Some potential complications of hypertension include:

* Heart disease (e.g., heart attacks, heart failure)
* Stroke
* Kidney disease (e.g., chronic kidney disease, end-stage renal disease)
* Vision loss (e.g., retinopathy)
* Peripheral artery disease

Hypertension is typically diagnosed through blood pressure readings taken over a period of time. Treatment for hypertension may include lifestyle changes (e.g., diet, exercise, stress management), medications, or a combination of both. The goal of treatment is to reduce the risk of complications and improve quality of life.

In medical terminology, nausea is sometimes used interchangeably with the term "dyspepsia," which refers to a general feeling of discomfort or unease in the stomach, often accompanied by symptoms such as bloating, belching, or heartburn. However, while nausea and dyspepsia can be related, they are not always the same thing, and it's important to understand the specific underlying cause of any gastrointestinal symptoms in order to provide appropriate treatment.

Some common causes of nausea include:

* Gastrointestinal disorders such as irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), and gastritis
* Motion sickness or seasickness
* Medication side effects, including chemotherapy drugs, antibiotics, and painkillers
* Pregnancy and morning sickness
* Food poisoning or other infections
* Migraines and other headaches
* Anxiety and stress

Treatment for nausea will depend on the underlying cause, but may include medications such as antihistamines, anticholinergics, or anti-nausea drugs, as well as non-pharmacological interventions such as ginger, acupressure, or relaxation techniques. In severe cases, hospitalization may be necessary to manage symptoms and prevent dehydration or other complications.

Myocardial ischemia can be caused by a variety of factors, including coronary artery disease, high blood pressure, diabetes, and smoking. It can also be triggered by physical exertion or stress.

There are several types of myocardial ischemia, including:

1. Stable angina: This is the most common type of myocardial ischemia, and it is characterized by a predictable pattern of chest pain that occurs during physical activity or emotional stress.
2. Unstable angina: This is a more severe type of myocardial ischemia that can occur without any identifiable trigger, and can be accompanied by other symptoms such as shortness of breath or vomiting.
3. Acute coronary syndrome (ACS): This is a condition that includes both stable angina and unstable angina, and it is characterized by a sudden reduction in blood flow to the heart muscle.
4. Heart attack (myocardial infarction): This is a type of myocardial ischemia that occurs when the blood flow to the heart muscle is completely blocked, resulting in damage or death of the cardiac tissue.

Myocardial ischemia can be diagnosed through a variety of tests, including electrocardiograms (ECGs), stress tests, and imaging studies such as echocardiography or cardiac magnetic resonance imaging (MRI). Treatment options for myocardial ischemia include medications such as nitrates, beta blockers, and calcium channel blockers, as well as lifestyle changes such as quitting smoking, losing weight, and exercising regularly. In severe cases, surgical procedures such as coronary artery bypass grafting or angioplasty may be necessary.

MRI can occur in various cardiovascular conditions, such as myocardial infarction (heart attack), cardiac arrest, and cardiac surgery. The severity of MRI can range from mild to severe, depending on the extent and duration of the ischemic event.

The pathophysiology of MRI involves a complex interplay of various cellular and molecular mechanisms. During ischemia, the heart muscle cells undergo changes in energy metabolism, electrolyte balance, and cell membrane function. When blood flow is restored, these changes can lead to an influx of calcium ions into the cells, activation of enzymes, and production of reactive oxygen species (ROS), which can damage the cells and their membranes.

The clinical presentation of MRI can vary depending on the severity of the injury. Some patients may experience chest pain, shortness of breath, and fatigue. Others may have more severe symptoms, such as cardiogenic shock or ventricular arrhythmias. The diagnosis of MRI is based on a combination of clinical findings, electrocardiography (ECG), echocardiography, and cardiac biomarkers.

The treatment of MRI is focused on addressing the underlying cause of the injury and managing its symptoms. For example, in patients with myocardial infarction, thrombolysis or percutaneous coronary intervention may be used to restore blood flow to the affected area. In patients with cardiac arrest, cardiopulmonary resuscitation (CPR) and other life-saving interventions may be necessary.

Prevention of MRI is crucial in reducing its incidence and severity. This involves aggressive risk factor management, such as controlling hypertension, diabetes, and dyslipidemia, as well as smoking cessation and stress reduction. Additionally, patients with a history of MI should adhere to their medication regimen, which may include beta blockers, ACE inhibitors or ARBs, statins, and aspirin.

In conclusion, myocardial injury with ST-segment elevation (MRI) is a life-threatening condition that requires prompt recognition and treatment. While the clinical presentation can vary depending on the severity of the injury, early diagnosis and management are crucial in reducing morbidity and mortality. Prevention through aggressive risk factor management and adherence to medication regimens is also essential in preventing MRI.

The term "decerebrate" comes from the Latin word "cerebrum," which means brain. In this context, the term refers to a state where the brain is significantly damaged or absent, leading to a loss of consciousness and other cognitive functions.

Some common symptoms of the decerebrate state include:

* Loss of consciousness
* Flaccid paralysis (loss of muscle tone)
* Dilated pupils
* Lack of responsiveness to stimuli
* Poor or absent reflexes
* Inability to speak or communicate

The decerebrate state can be caused by a variety of factors, including:

* Severe head injury
* Stroke or cerebral vasculature disorders
* Brain tumors or cysts
* Infections such as meningitis or encephalitis
* Traumatic brain injury

Treatment for the decerebrate state is typically focused on addressing the underlying cause of the condition. This may involve medications to control seizures, antibiotics for infections, or surgery to relieve pressure on the brain. In some cases, the decerebrate state may be a permanent condition, and individuals may require long-term care and support.

There are several causes of hypotension, including:

1. Dehydration: Loss of fluids and electrolytes can cause a drop in blood pressure.
2. Blood loss: Losing too much blood can lead to hypotension.
3. Medications: Certain medications, such as diuretics and beta-blockers, can lower blood pressure.
4. Heart conditions: Heart failure, cardiac tamponade, and arrhythmias can all cause hypotension.
5. Endocrine disorders: Hypothyroidism (underactive thyroid) and adrenal insufficiency can cause low blood pressure.
6. Vasodilation: A condition where the blood vessels are dilated, leading to low blood pressure.
7. Sepsis: Severe infection can cause hypotension.

Symptoms of hypotension can include:

1. Dizziness and lightheadedness
2. Fainting or passing out
3. Weakness and fatigue
4. Confusion and disorientation
5. Pale, cool, or clammy skin
6. Fast or weak pulse
7. Shortness of breath
8. Nausea and vomiting

If you suspect that you or someone else is experiencing hypotension, it is important to seek medical attention immediately. Treatment will depend on the underlying cause of the condition, but may include fluids, electrolytes, and medication to raise blood pressure. In severe cases, hospitalization may be necessary.

Reperfusion injury can cause inflammation, cell death, and impaired function in the affected tissue or organ. The severity of reperfusion injury can vary depending on the duration and severity of the initial ischemic event, as well as the promptness and effectiveness of treatment to restore blood flow.

Reperfusion injury can be a complicating factor in various medical conditions, including:

1. Myocardial infarction (heart attack): Reperfusion injury can occur when blood flow is restored to the heart muscle after a heart attack, leading to inflammation and cell death.
2. Stroke: Reperfusion injury can occur when blood flow is restored to the brain after an ischemic stroke, leading to inflammation and damage to brain tissue.
3. Organ transplantation: Reperfusion injury can occur when a transplanted organ is subjected to ischemia during harvesting or preservation, and then reperfused with blood.
4. Peripheral arterial disease: Reperfusion injury can occur when blood flow is restored to a previously occluded peripheral artery, leading to inflammation and damage to the affected tissue.

Treatment of reperfusion injury often involves medications to reduce inflammation and oxidative stress, as well as supportive care to manage symptoms and prevent further complications. In some cases, experimental therapies such as stem cell transplantation or gene therapy may be used to promote tissue repair and regeneration.

Body weight is an important health indicator, as it can affect an individual's risk for certain medical conditions, such as obesity, diabetes, and cardiovascular disease. Maintaining a healthy body weight is essential for overall health and well-being, and there are many ways to do so, including a balanced diet, regular exercise, and other lifestyle changes.

There are several ways to measure body weight, including:

1. Scale: This is the most common method of measuring body weight, and it involves standing on a scale that displays the individual's weight in kg or lb.
2. Body fat calipers: These are used to measure body fat percentage by pinching the skin at specific points on the body.
3. Skinfold measurements: This method involves measuring the thickness of the skin folds at specific points on the body to estimate body fat percentage.
4. Bioelectrical impedance analysis (BIA): This is a non-invasive method that uses electrical impulses to measure body fat percentage.
5. Dual-energy X-ray absorptiometry (DXA): This is a more accurate method of measuring body composition, including bone density and body fat percentage.

It's important to note that body weight can fluctuate throughout the day due to factors such as water retention, so it's best to measure body weight at the same time each day for the most accurate results. Additionally, it's important to use a reliable scale or measuring tool to ensure accurate measurements.

Hyperkinesis can manifest in different ways, including:

1. Excessive movement or restlessness: This can include fidgeting, pacing, or other forms of constant motion.
2. Involuntary movements: These can include tremors, tics, or other sudden, uncontrolled movements.
3. Overactive behavior: This can include rapid speaking, excessive talking, or other behaviors that are not typical for the individual.
4. Difficulty sitting still or remaining quiet: This can be due to an inability to focus or a sense of inner restlessness or agitation.
5. Increased energy levels: This can result in excessive physical activity, such as running, jumping, or other forms of high-energy behavior.

Hyperkinesis can have a significant impact on daily life, making it difficult to focus, complete tasks, and maintain relationships. It is important to seek medical attention if symptoms persist or worsen over time, as hyperkinesis can be a sign of an underlying neurological or psychiatric condition that requires treatment.

Pruritus can be acute or chronic, depending on its duration and severity. Acute pruritus is usually caused by a specific trigger, such as an allergic reaction or insect bite, and resolves once the underlying cause is treated or subsides. Chronic pruritus, on the other hand, can persist for months or even years and may be more challenging to diagnose and treat.

Some common causes of pruritus include:

1. Skin disorders such as atopic dermatitis, psoriasis, eczema, and contact dermatitis.
2. Allergic reactions to medications, insect bites, or food.
3. Certain systemic diseases such as kidney disease, liver disease, and thyroid disorders.
4. Pregnancy-related itching (obstetric pruritus).
5. Cancer and its treatment, particularly chemotherapy-induced itching.
6. Nerve disorders such as peripheral neuropathy and multiple sclerosis.
7. Infections such as fungal, bacterial, or viral infections.
8. Parasitic infestations such as scabies and lice.

Managing pruritus can be challenging, as it often leads to a vicious cycle of scratching and skin damage, which can exacerbate the itching sensation. Treatment options for pruritus depend on the underlying cause, but may include topical corticosteroids, oral antihistamines, immunomodulatory drugs, and other medications. In severe cases, hospitalization may be necessary to address the underlying condition and provide symptomatic relief.

In conclusion, pruritus is a common symptom with many possible causes, ranging from skin disorders to systemic diseases and infections. Diagnosis and management of pruritus require a comprehensive approach, involving both physical examination and laboratory tests to identify the underlying cause, as well as appropriate treatment options to provide relief and prevent complications.

Example Sentence: The patient was diagnosed with pulmonary hypertension and began treatment with medication to lower her blood pressure and improve her symptoms.

Word class: Noun phrase / medical condition

The term ischemia refers to the reduction of blood flow, and it is often used interchangeably with the term stroke. However, not all strokes are caused by ischemia, as some can be caused by other factors such as bleeding in the brain. Ischemic stroke accounts for about 87% of all strokes.

There are different types of brain ischemia, including:

1. Cerebral ischemia: This refers to the reduction of blood flow to the cerebrum, which is the largest part of the brain and responsible for higher cognitive functions such as thought, emotion, and voluntary movement.
2. Cerebellar ischemia: This refers to the reduction of blood flow to the cerebellum, which is responsible for coordinating and regulating movement, balance, and posture.
3. Brainstem ischemia: This refers to the reduction of blood flow to the brainstem, which is responsible for controlling many of the body's automatic functions such as breathing, heart rate, and blood pressure.
4. Territorial ischemia: This refers to the reduction of blood flow to a specific area of the brain, often caused by a blockage in a blood vessel.
5. Global ischemia: This refers to the reduction of blood flow to the entire brain, which can be caused by a cardiac arrest or other systemic conditions.

The symptoms of brain ischemia can vary depending on the location and severity of the condition, but may include:

1. Weakness or paralysis of the face, arm, or leg on one side of the body
2. Difficulty speaking or understanding speech
3. Sudden vision loss or double vision
4. Dizziness or loss of balance
5. Confusion or difficulty with memory
6. Seizures
7. Slurred speech or inability to speak
8. Numbness or tingling sensations in the face, arm, or leg
9. Vision changes, such as blurred vision or loss of peripheral vision
10. Difficulty with coordination and balance.

It is important to seek medical attention immediately if you experience any of these symptoms, as brain ischemia can cause permanent damage or death if left untreated.

Morphine dependence can occur after taking the drug for a short or long period, and it is often seen in individuals who use morphine for chronic pain management. The risk of developing morphine dependence increases with higher doses and longer durations of use.

Signs and symptoms of morphine dependence may include:

1. Increased tolerance to the drug, requiring higher doses to achieve the same effect.
2. Withdrawal symptoms when stopping or reducing the drug, such as anxiety, restlessness, muscle and bone pain, sweating, and insomnia.
3. Compulsive drug-seeking behavior, such as doctor shopping or stealing medication to maintain a supply of morphine.
4. Neglect of responsibilities and activities due to the pursuit of morphine use.
5. Continued use despite negative consequences, such as relationship problems, financial issues, or legal troubles.
6. Feeling a strong need or craving for morphine, which can be difficult to control.
7. Experiencing withdrawal symptoms when stopping or reducing the drug, such as nausea, vomiting, diarrhea, and tremors.
8. Developing tolerance to other opioids, which can lead to a cycle of increasing doses and dependence on multiple drugs.
9. Feeling irritable, anxious, or depressed when unable to obtain morphine.
10. Engaging in risky behaviors, such as sharing needles or using unregulated sources of the drug, which can increase the risk of overdose or infection.

Morphine dependence is a serious condition that can have significant negative consequences on an individual's physical and mental health, relationships, and overall quality of life. Treatment options for morphine dependence include medication-assisted therapy, counseling, and support groups to help individuals manage withdrawal symptoms and cravings, as well as address any underlying psychological or social issues that may be contributing to the addiction.

The different types of Neurotoxicity Syndromes include:

1. Organophosphate-induced neurotoxicity: This syndrome is caused by exposure to organophosphate pesticides, which can damage the nervous system and cause symptoms such as headaches, dizziness, and memory loss.
2. Heavy metal neurotoxicity: Exposure to heavy metals, such as lead, mercury, and arsenic, can damage the nervous system and cause symptoms such as tremors, muscle weakness, and cognitive impairment.
3. Pesticide-induced neurotoxicity: This syndrome is caused by exposure to pesticides, which can damage the nervous system and cause symptoms such as headaches, dizziness, and memory loss.
4. Solvent-induced neurotoxicity: Exposure to solvents, such as toluene and benzene, can damage the nervous system and cause symptoms such as memory loss, difficulty with concentration, and mood changes.
5. Medication-induced neurotoxicity: Certain medications, such as antidepressants and antipsychotics, can damage the nervous system and cause symptoms such as tremors, muscle rigidity, and cognitive impairment.
6. Environmental neurotoxicity: Exposure to environmental toxins, such as air pollution and pesticides, can damage the nervous system and cause symptoms such as headaches, dizziness, and memory loss.
7. Neurodegenerative disease-induced neurotoxicity: Neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease, can cause neurotoxicity and lead to symptoms such as cognitive decline, memory loss, and motor dysfunction.
8. Traumatic brain injury-induced neurotoxicity: Traumatic brain injury can cause neurotoxicity and lead to symptoms such as cognitive impairment, memory loss, and mood changes.
9. Stroke-induced neurotoxicity: A stroke can cause neurotoxicity and lead to symptoms such as weakness or paralysis on one side of the body, difficulty with speech and language, and memory loss.
10. Neurodevelopmental disorder-induced neurotoxicity: Neurodevelopmental disorders, such as autism spectrum disorder, can cause neurotoxicity and lead to symptoms such as cognitive impairment, social withdrawal, and repetitive behaviors.

It is important to note that these are just a few examples of the many different types of neurotoxicity that can occur, and that each type may have its own unique set of causes, symptoms, and treatments. If you suspect that you or someone you know may be experiencing neurotoxicity, it is important to seek medical attention as soon as possible in order to receive an accurate diagnosis and appropriate treatment.

There are several types of ischemia, including:

1. Myocardial ischemia: Reduced blood flow to the heart muscle, which can lead to chest pain or a heart attack.
2. Cerebral ischemia: Reduced blood flow to the brain, which can lead to stroke or cognitive impairment.
3. Peripheral arterial ischemia: Reduced blood flow to the legs and arms.
4. Renal ischemia: Reduced blood flow to the kidneys.
5. Hepatic ischemia: Reduced blood flow to the liver.

Ischemia can be diagnosed through a variety of tests, including electrocardiograms (ECGs), stress tests, and imaging studies such as CT or MRI scans. Treatment for ischemia depends on the underlying cause and may include medications, lifestyle changes, or surgical interventions.

Asthma can cause recurring episodes of wheezing, coughing, chest tightness, and shortness of breath. These symptoms occur when the muscles surrounding the airways contract, causing the airways to narrow and swell. This can be triggered by exposure to environmental allergens or irritants such as pollen, dust mites, pet dander, or respiratory infections.

There is no cure for asthma, but it can be managed with medication and lifestyle changes. Treatment typically includes inhaled corticosteroids to reduce inflammation, bronchodilators to open up the airways, and rescue medications to relieve symptoms during an asthma attack.

Asthma is a common condition that affects people of all ages, but it is most commonly diagnosed in children. According to the American Lung Association, more than 25 million Americans have asthma, and it is the third leading cause of hospitalization for children under the age of 18.

While there is no cure for asthma, early diagnosis and proper treatment can help manage symptoms and improve quality of life for those affected by the condition.

The inner ear, brain, and sensory nerves are all involved in the development of motion sickness. The inner ear contains the vestibular system, which is responsible for maintaining balance and equilibrium. The brain processes visual, proprioceptive (position and movement), and vestibular information to determine the body's position and movement. When these signals are not in harmony, the brain can become confused and motion sickness can occur.

There are several factors that can contribute to the development of motion sickness, including:

1. Conflicting sensory input: This can occur when the visual, proprioceptive, and vestibular systems provide conflicting information about the body's position and movement. For example, if the body is moving but the eyes do not see any movement, this can confuse the brain and lead to motion sickness.
2. Movement of the body: Motion sickness can occur when the body is in motion, such as on a boat or airplane, or during a car ride. This can be particularly problematic for people who are prone to motion sickness.
3. Reading or looking at screens: Reading or looking at screens can exacerbate motion sickness, as it can provide conflicting visual and vestibular information.
4. Other medical conditions: Certain medical conditions, such as inner ear problems or migraines, can increase the risk of developing motion sickness.
5. Medications: Some medications, such as antidepressants and antihistamines, can increase the risk of developing motion sickness.

There are several ways to prevent and treat motion sickness, including:

1. Avoiding heavy meals before traveling: Eating a light meal before traveling can help reduce the risk of motion sickness.
2. Choosing a seat with less motion: In vehicles, choosing a seat with less motion can help reduce the risk of motion sickness.
3. Keeping the eyes on the horizon: Looking at the horizon can help reduce the conflict between visual and vestibular information.
4. Taking medication: There are several over-the-counter and prescription medications available to prevent and treat motion sickness, such as dramamine and scopolamine patches.
5. Using wristbands: Sea bands or wristbands that apply pressure to a specific point on the wrist have been shown to be effective in preventing motion sickness.
6. Avoiding alcohol and caffeine: Consuming these substances can exacerbate motion sickness, so it is best to avoid them before and during travel.
7. Staying hydrated: Drinking plenty of water and other fluids can help reduce the symptoms of motion sickness.
8. Getting fresh air: Fresh air can help reduce the symptoms of motion sickness, so it is best to sit near an open window or take breaks outside.

* Heart block: A condition where the electrical signals that control the heart's rhythm are blocked or delayed, leading to a slow heart rate.
* Sinus node dysfunction: A condition where the sinus node, which is responsible for setting the heart's rhythm, is not functioning properly, leading to a slow heart rate.
* Medications: Certain medications, such as beta blockers, can slow down the heart rate.
* Heart failure: In severe cases of heart failure, the heart may become so weak that it cannot pump blood effectively, leading to a slow heart rate.
* Electrolyte imbalance: An imbalance of electrolytes, such as potassium or magnesium, can affect the heart's ability to function properly and cause a slow heart rate.
* Other medical conditions: Certain medical conditions, such as hypothyroidism (an underactive thyroid) or anemia, can cause bradycardia.

Bradycardia can cause symptoms such as:

* Fatigue
* Weakness
* Dizziness or lightheadedness
* Shortness of breath
* Chest pain or discomfort

In some cases, bradycardia may not cause any noticeable symptoms at all.

If you suspect you have bradycardia, it is important to consult with a healthcare professional for proper diagnosis and treatment. They may perform tests such as an electrocardiogram (ECG) or stress test to determine the cause of your slow heart rate and develop an appropriate treatment plan. Treatment options for bradycardia may include:

* Medications: Such as atropine or digoxin, to increase the heart rate.
* Pacemakers: A small device that is implanted in the chest to help regulate the heart's rhythm and increase the heart rate.
* Cardiac resynchronization therapy (CRT): A procedure that involves implanting a device that helps both ventricles of the heart beat together, improving the heart's pumping function.

It is important to note that bradycardia can be a symptom of an underlying condition, so it is important to address the underlying cause in order to effectively treat the bradycardia.

There are different types of myocardial infarctions, including:

1. ST-segment elevation myocardial infarction (STEMI): This is the most severe type of heart attack, where a large area of the heart muscle is damaged. It is characterized by a specific pattern on an electrocardiogram (ECG) called the ST segment.
2. Non-ST-segment elevation myocardial infarction (NSTEMI): This type of heart attack is less severe than STEMI, and the damage to the heart muscle may not be as extensive. It is characterized by a smaller area of damage or a different pattern on an ECG.
3. Incomplete myocardial infarction: This type of heart attack is when there is some damage to the heart muscle but not a complete blockage of blood flow.
4. Collateral circulation myocardial infarction: This type of heart attack occurs when there are existing collateral vessels that bypass the blocked coronary artery, which reduces the amount of damage to the heart muscle.

Symptoms of a myocardial infarction can include chest pain or discomfort, shortness of breath, lightheadedness, and fatigue. These symptoms may be accompanied by anxiety, fear, and a sense of impending doom. In some cases, there may be no noticeable symptoms at all.

Diagnosis of myocardial infarction is typically made based on a combination of physical examination findings, medical history, and diagnostic tests such as an electrocardiogram (ECG), cardiac enzyme tests, and imaging studies like echocardiography or cardiac magnetic resonance imaging.

Treatment of myocardial infarction usually involves medications to relieve pain, reduce the amount of work the heart has to do, and prevent further damage to the heart muscle. These may include aspirin, beta blockers, ACE inhibitors or angiotensin receptor blockers, and statins. In some cases, a procedure such as angioplasty or coronary artery bypass surgery may be necessary to restore blood flow to the affected area.

Prevention of myocardial infarction involves managing risk factors such as high blood pressure, high cholesterol, smoking, diabetes, and obesity. This can include lifestyle changes such as a healthy diet, regular exercise, and stress reduction, as well as medications to control these conditions. Early detection and treatment of heart disease can help prevent myocardial infarction from occurring in the first place.

Neuralgia is often difficult to diagnose and treat, as the underlying cause can be challenging to identify. However, various medications and therapies can help manage the pain and other symptoms associated with this condition. These may include pain relievers, anticonvulsants, antidepressants, and muscle relaxants, as well as alternative therapies such as acupuncture or physical therapy.

Some common forms of neuralgia include:

1. Trigeminal neuralgia: This is a condition that affects the trigeminal nerve, which carries sensation from the face to the brain. It is characterized by sudden, intense pain in the face, typically on one side.
2. Postherpetic neuralgia (PHN): This is a condition that occurs after a shingles infection, and is characterized by persistent pain in the affected area.
3. Occipital neuralgia: This is a condition that affects the nerves in the back of the head and neck, and can cause pain in the back of the head, neck, and face.
4. Geniculate neuralgia: This is a rare condition that affects the nerves in the jaw and ear, and can cause pain in the jaw, face, and ear.

Overall, neuralgia is a complex and debilitating condition that can significantly impact an individual's quality of life. It is important for individuals experiencing symptoms of neuralgia to seek medical attention to determine the underlying cause and develop an appropriate treatment plan.

Hypothermia can be mild, moderate, or severe. Mild hypothermia is characterized by shivering and a body temperature of 95 to 97 degrees Fahrenheit (32 to 36.1 degrees Celsius). Moderate hypothermia has a body temperature of 82 to 94 degrees Fahrenheit (28 to 34 degrees Celsius), and the person may appear lethargic, drowsy, or confused. Severe hypothermia is characterized by a body temperature below 82 degrees Fahrenheit (28 degrees Celsius) and can lead to coma and even death if not treated promptly.

Treatment for hypothermia typically involves warming the person up slowly, using blankets or heating pads, and providing warm fluids to drink. In severe cases, medical professionals may use a specialized warm water bath or apply warm packs to specific areas of the body.

Preventing hypothermia is important, especially in cold weather conditions. This can be done by dressing appropriately for the weather, staying dry and avoiding wet clothing, eating regularly to maintain energy levels, and seeking shelter if you become stranded or lost. It's also essential to recognize the signs of hypothermia early on so that treatment can begin promptly.

1. Cocaine dependence: This is a condition in which an individual becomes psychologically and physiologically dependent on cocaine, and experiences withdrawal symptoms when they stop using the drug.
2. Cocaine intoxication: This is a state of altered consciousness that can occur when an individual takes too much cocaine, and can cause symptoms such as agitation, confusion, and hallucinations.
3. Cocaine-induced psychosis: This is a condition in which an individual experiences a break from reality, characterized by delusions, hallucinations, and disorganized thinking.
4. Cocaine-associated cardiovascular problems: Cocaine use can increase heart rate and blood pressure, and can cause damage to the heart and blood vessels.
5. Cocaine-associated respiratory problems: Cocaine use can constrict the airways and make breathing more difficult, which can lead to respiratory failure.
6. Cocaine-associated neurological problems: Cocaine use can cause nerve damage and seizures, particularly in individuals who use the drug frequently or in large quantities.
7. Cocaine withdrawal syndrome: This is a set of symptoms that can occur when an individual stops using cocaine, including depression, anxiety, and fatigue.
8. Cocaine-related anxiety disorders: Cocaine use can exacerbate anxiety disorders such as generalized anxiety disorder, panic disorder, and social anxiety disorder.
9. Cocaine-related mood disorders: Cocaine use can also exacerbate mood disorders such as depression and bipolar disorder.
10. Cocaine-related cognitive impairment: Chronic cocaine use can impair cognitive function, particularly in areas such as attention, memory, and decision-making.

It is important to note that the effects of cocaine can vary depending on the individual, the dose and frequency of use, and other factors such as the method of administration and any underlying medical conditions. If you or someone you know is struggling with cocaine addiction, it is important to seek professional help as soon as possible.

A type of hypertension that is caused by a problem with the kidneys. It can be acute or chronic and may be associated with other conditions such as glomerulonephritis, pyelonephritis, or polycystic kidney disease. Symptoms include proteinuria, hematuria, and elevated blood pressure. Treatment options include diuretics, ACE inhibitors, and angiotensin II receptor blockers.

Note: Renal hypertension is also known as renal artery hypertension.

Types of Experimental Diabetes Mellitus include:

1. Streptozotocin-induced diabetes: This type of EDM is caused by administration of streptozotocin, a chemical that damages the insulin-producing beta cells in the pancreas, leading to high blood sugar levels.
2. Alloxan-induced diabetes: This type of EDM is caused by administration of alloxan, a chemical that also damages the insulin-producing beta cells in the pancreas.
3. Pancreatectomy-induced diabetes: In this type of EDM, the pancreas is surgically removed or damaged, leading to loss of insulin production and high blood sugar levels.

Experimental Diabetes Mellitus has several applications in research, including:

1. Testing new drugs and therapies for diabetes treatment: EDM allows researchers to evaluate the effectiveness of new treatments on blood sugar control and other physiological processes.
2. Studying the pathophysiology of diabetes: By inducing EDM in animals, researchers can study the progression of diabetes and its effects on various organs and tissues.
3. Investigating the role of genetics in diabetes: Researchers can use EDM to study the effects of genetic mutations on diabetes development and progression.
4. Evaluating the efficacy of new diagnostic techniques: EDM allows researchers to test new methods for diagnosing diabetes and monitoring blood sugar levels.
5. Investigating the complications of diabetes: By inducing EDM in animals, researchers can study the development of complications such as retinopathy, nephropathy, and cardiovascular disease.

In conclusion, Experimental Diabetes Mellitus is a valuable tool for researchers studying diabetes and its complications. The technique allows for precise control over blood sugar levels and has numerous applications in testing new treatments, studying the pathophysiology of diabetes, investigating the role of genetics, evaluating new diagnostic techniques, and investigating complications.

Synonyms: Bronchial Constriction, Airway Spasm, Reversible Airway Obstruction.

Antonyms: Bronchodilation, Relaxation of Bronchial Muscles.

Example Sentences:

1. The patient experienced bronchial spasms during the asthma attack and was treated with an inhaler.
2. The bronchial spasm caused by the allergic reaction was relieved by administering epinephrine.
3. The doctor prescribed corticosteroids to reduce inflammation and prevent future bronchial spasms.

Schwabe U, Ukena D, Lohse MJ (September 1985). "Xanthine derivatives as antagonists at A1 and A2 adenosine receptors". Naunyn- ... v t e (ECHA InfoCard ID from Wikidata, Drugboxes which contain changes to watched fields, Adenosine receptor antagonists, Diols ... It acts as an adenosine receptor antagonist and phosphodiesterase inhibitor. Xanthine "International Non-Proprietary Names. ...
... activity as antagonists of A1- and A2-adenosine receptors". Biochemical Pharmacology. 37 (4): 655-64. doi:10.1016/0006-2952(88) ... Adenosine receptor antagonists, Amines, Ethyl esters, Carboxylate esters, GABAA receptor positive allosteric modulators, ... It is also known to act as an adenosine antagonist at the A1 and A2 subtypes and as a phosphodiesterase inhibitor. Cartazolate ... "Perturbation of benzodiazepine receptor binding by pyrazolopyridines involves picrotoxinin/barbiturate receptor sites". Journal ...
In order to be able to characterize the function of adenosine A2 receptors, potent and selective A2-receptor antagonists were ... Adenosine A2A receptor antagonists are a class of drugs that blocks adenosine at the adenosine A2A receptor. Notable adenosine ... adenosine receptor antagonists as potential therapeutics, antagonist for A2A-receptors, adenosine receptor ligands as anti- ... In order to achieve high affinity at adenosine receptors, certain criteria must be fulfilled. Adenosine receptor antagonists, ...
... a potent and selective adenosine A2 receptor antagonist". European Journal of Pharmacology. 267 (3): 335-41. doi:10.1016/0922- ... Older research on adenosine receptor function, and non-selective adenosine receptor antagonists such as aminophylline, focused ... As a result, Adenosine receptor A2A decreases activity in the Dopamine D2 receptors. The adenosine A2A receptor has also been ... "Chromosomal mapping of A1 and A2 adenosine receptors, VIP receptor, and a new subtype of serotonin receptor". Genomics. 11 (1 ...
"Comparison of the behavioural effects of an adenosine A1/A2-receptor antagonist, CGS 15943A, and an A1-selective antagonist, ... CGS-15943 is a drug which acts as a potent and reasonably selective antagonist for the adenosine receptors A1 and A2A, having a ... It was one of the first adenosine receptor antagonists discovered that is not a xanthine derivative, instead being a ... Holtzman SG (1991). "CGS 15943, a nonxanthine adenosine receptor antagonist: effects on locomotor activity of nontolerant and ...
March 2002). "BG9719 (CVT-124), an A1 adenosine receptor antagonist, protects against the decline in renal function observed ... Caffeine may reduce cerebral blood flow in premature infants, it is presumed by blocking vascular A2 ARs. Thus, it may prove ... The adenosine A1 receptor is one member of the adenosine receptor group of G protein-coupled receptors with adenosine as ... The adenosine A1 receptor has been found to be ubiquitous throughout the entire body. Activation of the adenosine A1 receptor ...
... is a caffeine analog which displays affinity to A2 adenosine receptors, in contrast to the A1 subtype receptors. DMPX had 28× ... Adenosine receptor antagonists, Anxiogenics, Caffeine, Designer drugs, Vasoconstrictors, Propargyl compounds). ... a potent and selective in vivo antagonist of adenosine analogs". Life Sciences. 43 (21): 1671-84. doi:10.1016/0024-3205(88) ...
These signaling elements include thromboxane A2, receptor type α, phospholipase Cβ3, and IP3 receptors. Signalization in ... It belongs to the homologous family of glycoprotein IIb-IIa antagonists. Kistrin has an adhesion site that binds to GP IIb-IIIa ... cAMP, cyclic adenosine monophosphate, phosphorylate messengers via protein kinase A (PKA). ... TX2 effects are mediated by G protein-coupled receptors, subtypes TPα and TPβ. Both receptors mediate phospholipase C ...
GABAA receptor positive allosteric modulators, Adenosine receptor antagonists). ... as an adenosine antagonist of the A1 and A2 subtypes, and as a phosphodiesterase inhibitor selective for the PDE4 isoform. It ... ISBN 3-7643-1837-6. Williams M, Jarvis MF (February 1988). "Adenosine antagonists as potential therapeutic agents". ... Zezula J, Slany A, Sieghart W (April 1996). "Interaction of allosteric ligands with GABAA receptors containing one, two, or ...
Asapiprant (S-555739) and Laropiprant are selective receptor antagonists of DP1 whereas Vidupiprant is a receptor antagonist ... the DP1-dependent stimulation of adenosine formation and subsequent simulation of the Adenosine A2A receptor by adenosine. In ... thromboxane A2, with PGD2 being more than 100-fold more potent than PGE2 in binding to and stimulating DP1. (http://www. ... Prostaglandin receptors Prostanoid receptors Prostaglandin DP2 receptor Eicosanoid receptor GRCh38: Ensembl release 89: ...
"Stimulation of high-affinity adenosine A2 receptors decreases the affinity of dopamine D2 receptors in rat striatal membranes ... "Structures of the CXCR4 chemokine GPCR with small-molecule and cyclic peptide antagonists". Science. 330 (6007): 1066-71. ... In 1991, the phenomenon of receptor crosstalk was observed between adenosine A2A (A2A) and dopamine D2 receptor (DRD2) thus ... two adenosine A2A receptors and two dopamine D2 receptors). Maggio and co-workers showed in 1993 the ability of the muscarinic ...
... also partial agonist of µ-opioid receptors, and competitive antagonist of δ-opioid and κ-opioid receptors) BU08028 (Analogue of ... Fukuda K, Shoda T, Morikawa H, Kato S, Mima H, Mori K (1998). "Activation of phospholipase A2 by the nociceptin receptor ... causing an intracellular decrease in cyclic adenosine monophosphate(cAMP) levels, an important second messenger for many signal ... receptor or kappa-type 3 opioid receptor, is a protein that in humans is encoded by the OPRL1 (opioid receptor-like 1) gene. ...
... a novel specific adenosine A(3) receptor antagonist with adenosine A(3) receptor agonists both in vitro and in vivo". Eur. J. ... 1997). "Adenosine inhibits neutrophil degranulation in activated human whole blood: involvement of adenosine A2 and A3 ... a novel ligand that demonstrates both adenosine A(2A) receptor agonist and adenosine A(3) receptor antagonist activity". ... is an adenosine receptor, but also denotes the human gene encoding it. Adenosine A3 receptors are G protein-coupled receptors ...
The GPIIb/IIIa antagonist blocks the binding of fibrinogen to the GPIIb/IIIa receptors, preventing the formation of platelet- ... Adenosine diphosphate (ADP) is a platelet agonist. When it is added to saline-diluted whole blood in the test cuvette, it ... and PGH2 is then converted to thromboxane A2 (TXA2) by thromboxane synthase. TXA2 increases platelet aggregation, promotes ... Thrombin receptor activating peptide-6 (TRAP-6) activates platelets through the thrombin receptor protease activated receptor-1 ...
The A1 receptors couple to Gi/o and decreases cAMP levels, while the A2 adenosine receptors couple to Gs, which stimulates ... have a purine structure and bind to some of the same receptors as adenosine. Methylxanthines act as competitive antagonists of ... All adenosine receptor subtypes (A1, A2A, A2B, and A3) are G-protein-coupled receptors. The four receptor subtypes are further ... Adenosine is believed to be an anti-inflammatory agent at the A2A receptor. Topical treatment of adenosine to foot wounds in ...
"Chromosomal mapping of A1 and A2 adenosine receptors, VIP receptor, and a new subtype of serotonin receptor". Genomics. 11 (1 ... mixed 5-HT1B/1D antagonist) LY-310,762 LY-367,642 LY-456,219 LY-456,220 5-HT1 receptor 5-HT receptor GRCh38: Ensembl release 89 ... 5-hydroxytryptamine (serotonin) receptor 1D, also known as HTR1D, is a 5-HT receptor, but also denotes the human gene encoding ... 5HT1D receptor is a G protein linked receptor that activates an intracellular messenger cascade to produce an inhibitory ...
Yang Z, Sun W, Hu K (Apr 2012). "Molecular mechanism underlying adenosine receptor-mediated mitochondrial targeting of protein ... Perjés Á, Skoumal R, Tenhunen O, Kónyi A, Simon M, Horváth IG, Kerkelä R, Ruskoaho H, Szokodi I (2014). "Apelin increases ... Gray MO, Karliner JS, Mochly-Rosen D (Dec 1997). "A selective epsilon-protein kinase C antagonist inhibits protection of ... Yang Z, Sun W, Hu K (Apr 2012). "Molecular mechanism underlying adenosine receptor-mediated mitochondrial targeting of protein ...
... glutamate receptor antagonist on ethanol consumption by genetic drinking rats. Alcohol, 40, 494-497. Hodge, C.W., Miles, M.F., ... Katsura, M., Shibasaki, M., Hayashida, S., Torigoe, F., Tsujimura, A., Ohkuma, S. (2006) Increase in expression of a1 and a2/d1 ... Pandey, S.C., Roy, A., Zhang, H. (2003). The decreased phosphorylation of cyclic adenosine monophosphate (cAMP) response ... receptors are glutamate receptors particularly important in long-term potentiation in neurons. These receptors have been linked ...
D5 receptors show higher affinity for agonists and lower affinity for antagonists than D1 receptors. Dihydrexidine Rotigotine ... Prado C, Contreras F, González H, Díaz P, Elgueta D, Barrientos M, Herrada AA, Lladser Á, Bernales S, Pacheco R (2012). " ... Mello, F. G. (October 1978). "The Ontogeny of Dopamine-Dependent Increase of Adenosine 3',5'-Cyclic Monophosphate in the Chick ... It belongs to the D1-like receptor family along with the D1 receptor subtype. D5 receptor is a subtype of the dopamine receptor ...
It works by binding and activating the prostaglandin E2 receptor which results in the opening and softening of the cervix and ... PGE2 synthesis within the body begins with the activation of arachidonic acid (AA) by the enzyme phospholipase A2. Once ... It promotes vasodilation of smooth muscles by increasing the activity of cyclic adenosine monophosphate (cAMP) to decrease ... "A live imaging cell motility screen identifies prostaglandin E2 as a T cell stop signal antagonist". Journal of Immunology. 187 ...
... s secrete thromboxane A2, which acts on the platelet's own thromboxane receptors on the platelet surface (hence the so- ... Clopidogrel and related antiplatelet medications also work as purinergic receptor P2Y12 antagonists.[citation needed] Data ... "Differential Sensitivity of Various Markers of Platelet Activation with Adenosine Diphosphate". BioNanoScience. 9 (1): 53-58. ... These receptors trigger intraplatelet signaling, which converts GPIIb/IIIa receptors to their active form to initiate ...
Montelukast, Zafirlukast, and Pranlukast are receptor antagonists for the Cysteinyl leukotriene receptor 1 which contributes to ... The cytosolic PLA2 set (i.e. cPLA2s) of PLA2 enzymes (cPLA2; see Phospholipase A2#Cytosolic phospholipases A2) in particular ... may serve as a mobile lid over ALOX5's substrate-binding site An Adenosine triphosphate (ATP) binding site; ATP is crucial for ... as well as of LTC4 and LTD4 receptor antagonists have proven inferior to corticosteroids as single drug therapy for persistent ...
It is a platelet inhibitor and an irreversible antagonist of P2Y12 ADP receptors and is of the thienopyridine drug class. It ... Adenosine diphosphate receptor inhibitors, Eli Lilly and Company brands, Daiichi Sankyo, Fluoroarenes, Ketones, Thienopyridines ... Demcsák A, Lantos T, Bálint ER, Hartmann P, Vincze Á, Bajor J, et al. (2018-11-19). "PPIs Are Not Responsible for Elevating ... Baker WL, White CM (2009). "Role of prasugrel, a novel P2Y(12) receptor antagonist, in the management of acute coronary ...
... trienoic acid as a thromboxane A2 receptor antagonist with minimal intrinsic activity". British Journal of Haematology. 101 (1 ... to inhibit platelet aggregation responses to various agents by stimulating platelets to raise their levels of Cyclic adenosine ... BLT1 receptor) and its low affinity BLT2 receptor (Kd=23 nM); both receptors are G protein coupled receptors that, when ligand- ... Hicks, A; Monkarsh, S. P.; Hoffman, A. F.; Goodnow Jr, R (2007). "Leukotriene B4 receptor antagonists as therapeutics for ...
... s have largely superseded the H2-receptor antagonists, a group of medications with similar effects but a ... Lucendo AJ, Arias Á, Molina-Infante J (January 2016). "Efficacy of Proton Pump Inhibitor Drugs for Inducing Clinical and ... Proton pump inhibitors act by irreversibly blocking the hydrogen/potassium adenosine triphosphatase enzyme system (the H+/K+ ... H2-receptor antagonists and prokinetics for gastro-oesophageal reflux disease-like symptoms and endoscopy negative reflux ...
Most commonly, enzymes known as adenosine deaminases acting on RNA (ADARs) catalyze adenosine to inosine (A to I) transitions. ... miR-382 is the target for the dopamine receptor D1 (DRD1), and its overexpression results in the upregulation of DRD1 and delta ... The specific microRNA, miR-506 has been found to work as a tumor antagonist in several studies. A significant number of ... "High mobility group A2 protein and its derivatives bind a specific region of the promoter of DNA repair gene ERCC1 and modulate ...
Alquezar C, Salado IG, de la Encarnación A, Pérez DI, Moreno F, Gil C, de Munain AL, Martínez A, Martín-Requero Á (April 2016 ... Elias L, Li AP, Longmire J (June 1981). "Cyclic adenosine 3':5'-monophosphate-dependent and -independent protein kinase in ... and to be antagonists of the Wnt pathway, show structural similarities to benzimidazole-based CK1 inhibitors, among them ... receptors, transport vesicles, components of the cytoskeleton, centrosomes or spindle poles. While the present NLS is not ...
... direct-acting Antagonist and indirect-acting Antagonists: Direct-acting antagonist- which takes up space present on receptors ... adenosine triphosphate (ATP), adenosine Others: acetylcholine (ACh), anandamide, etc. In addition, over 100 neuroactive ... Rinaman L (February 2011). "Hindbrain noradrenergic A2 neurons: diverse roles in autonomic, endocrine, cognitive, and ... An irreversible antagonist binds so strongly to the receptor as to render the receptor unavailable for binding to the agonist. ...
They are SRIs and litoxetine is also a 5-HT3 receptor antagonist while lubazodone is also a 5-HT2A receptor antagonist. In the ... One such possible mechanism is the increased levels of cyclic adenosine monophosphate (cAMP) as a result of interference with ... PMID 21701626.{{cite journal}}: CS1 maint: multiple names: authors list (link) Romero-Martínez Á, Murciano-Martí S, Moya-Albiol ... Fluvoxamine is an agonist of the σ1 receptor, while sertraline is an antagonist of the σ1 receptor, and paroxetine does not ...
IGF1R Interleukin 1 receptor antagonist deficiency; 612852; IL1RN Interleukin-2 receptor, alpha chain, deficiency of; 606367; ... IHH Brachydactyly type A2; 112600; BMPR1B Brachydactyly type A2; 112600; GDF5 Brachydactyly type B1; 113000; ROR2 Brachydactyly ... APC Adenosine deaminase deficiency, partial; 102700; ADA Adenosine triphosphate, elevated, of erythrocytes; 102900; PKLR ... associated with acetylcholine receptor deficiency; 608931; MUSK Myasthenic syndrome, congenital, associated with acetylcholine ...
Adenosine A2 Receptor Antagonists Actions. * Search in PubMed * Search in MeSH * Add to Search ... Brain adenosine A2A receptor occupancy by a novel A1/A2A receptor antagonist, ASP5854, in rhesus monkeys: relationship to ... Brain adenosine A2A receptor occupancy by a novel A1/A2A receptor antagonist, ASP5854, in rhesus monkeys: relationship to ... Adenosine A(2A) Receptor Antagonists and Parkinsons Disease. Shook BC, Jackson PF. Shook BC, et al. ACS Chem Neurosci. 2011 ...
Adenosine has strong immunosuppressive effects, many of which are mediated by A(2A) receptors (A(2A)R) ex … ... Adenosine levels are elevated during tissue hypoxia and damage associated with sepsis. ... Adenosine A2 Receptor Antagonists Actions. * Search in PubMed * Search in MeSH * Add to Search ... Improvement of the sepsis survival rate by adenosine 2a receptor antagonists depends on immune regulatory functions of ...
MeSH Terms: Adenosine A2 Receptor Antagonists/pharmacology*; Animals; Disease Models, Animal; Inflammation/metabolism; ... and suggest that some aspects of the neuroprotection observed with adenosine A2A receptor antagonists may involve direct or ... Title: Adenosine A2A receptor antagonism reverses inflammation-induced impairment of microglial process extension in a model of ... Pre-treatment of slices from MPTP-injected mice with the A2A receptor-selective antagonist preladenant restores the ability of ...
Binding of [3H]KF17837S, a selective adenosine A2 receptor antagonist, to rat brain membranes.. Nonaka H; Mori A; Ichimura M; ... 5. Effects of adenosine A1 and A2 receptor activation on electrically evoked dopamine and acetylcholine release from rat ... 1. Adenosine A1 receptor-mediated inhibition of dopamine release from rat striatal slices is modulated by D1 dopamine receptors ... 4. Activation of adenosine A1 receptor modulates dopamine D1 receptor activity in stably cotransfected human embryonic kidney ...
Adenosine A2 Receptor Antagonists [D27.505.519.625.725.400.100.200] * Adenosine A3 Receptor Antagonists [D27.505.519.625. ... Adenosine A2 Receptor Antagonists [D27.505.696.577.725.400.100.200] * Adenosine A3 Receptor Antagonists [D27.505.696.577. ... Adenosine A2B Receptor Antagonists Registry Number. 0. Previous Indexing. Receptors, Adenosine A2/antagonists & inhibitors ( ... Adenosine A2B Receptor Antagonists Narrower Concept UI. M0545365. Registry Number. 0. Terms. Adenosine A2B Receptor Antagonists ...
8460 Adenosine A2 receptor agonist 16326 Adenosine A2 receptor antagonist 35017 Adenosine A2a receptor agonist 24353 Adenosine ... A2a receptor antagonist 9116 Adenosine A3 receptor agonist 130827 Adenosine A3 receptor antagonist 13123 Adenosine deaminase ... 8501 Adenosine receptor agonist 21556 Adenosine receptor antagonist 40787 Adrenaline agonist 23473 Adrenaline antagonist 90977 ... 81942 GABA A receptor agonist 77515 GABA A receptor antagonist 98060 GABA B receptor agonist 64771 GABA B receptor antagonist ...
Antagonistes des récepteurs A2 à ladénosine Entry term(s):. Adenosine A2A Receptor Antagonists. Adenosine A2B Receptor ... Adenosine A2 Receptor Antagonists - Preferred Concept UI. M0545364. Scope note. Compounds that selectively bind to and block ... Compounds that selectively bind to and block the activation of ADENOSINE A2 RECEPTORS.. ... Adenosine A2 Receptor Antagonists [D27.505.519.625.725.400.100.200] Adenosine A2 Receptor Antagonists ...
Adenosine A2 Receptor Antagonists [D27.505.519.625.725.400.100.200] * Adenosine A3 Receptor Antagonists [D27.505.519.625. ... Adenosine A2 Receptor Antagonists [D27.505.696.577.725.400.100.200] * Adenosine A3 Receptor Antagonists [D27.505.696.577. ... Adenosine A2B Receptor Antagonists Registry Number. 0. Previous Indexing. Receptors, Adenosine A2/antagonists & inhibitors ( ... Adenosine A2B Receptor Antagonists Narrower Concept UI. M0545365. Registry Number. 0. Terms. Adenosine A2B Receptor Antagonists ...
... an adenosine A2 receptor antagonist, SCH58261 (1 and 3 mg/kg, i.p.) in combination with oseltamivir for 1 day increased ... a non-selective adenosine A1/A2 receptor antagonist, combined with oseltamivir. Oseltamivir is rapidly hydrolyzed to its active ... Agonistas del Receptor de Adenosina A2/farmacología , Antagonistas del Receptor de Adenosina A2/farmacología , Animales , ... Our findings suggest an interaction between the central blockade of adenosine A2 receptors by caffeine and OCB-induced ...
Adenosine with or without adenosine A1 and A2 receptor antagonists was applied to determine the efficacy and mechanism of ... or this concentration of adenosine plus the A1adenosine receptor antagonist DPCPX, 1 μm (Ad+DPCPX), or the A2adenosine receptor ... or this concentration of adenosine plus the A1adenosine receptor antagonist DPCPX, 1 μm (Ad+DPCPX), or the A2adenosine receptor ... In addition, adenosine receptor antagonists were used to study the role of adenosine receptor subtypes in altering glutamate ...
... by activation of adenosine A2A receptors (A2AR) is coupled to epoxyeicosatrienoic acid (EET) release. We have investigated the ... Receptors, Adenosine A2 / analysis * Receptors, Adenosine A2 / physiology* * Renal Artery / chemistry * Renal Artery / ... ADP Ribose Transferases / antagonists & inhibitors * ADP Ribose Transferases / physiology * Adenine / analogs & derivatives ... Dilation of rat preglomerular microvessels (PGMV) by activation of adenosine A2A receptors (A2AR) is coupled to ...
... receptors of adenosine, which has a protective effect on neuropathic pain in some doses by inhibiting A2a, A2b receptors. ... Caffeine is a non-selective antagonist of A1, A2a, ... Caffeine is a non-selective antagonist of A1, A2a, receptors of ... Adenosine A2A receptor antagonists are potential antidepressants: evidence based on pharmacology and A2A receptor knockout mice ... adenosine, which has a protective effect on neuropathic pain in some doses by inhibiting A2a, A2b receptors. Considering that ...
Adenosine A2 Receptor Agonists. Receptors, Adenosine A2/antagonists & inhibitors. Adenosine A2 Receptor Antagonists ... Receptor, Adenosine A3/antagonists & inhibitors. Adenosine A3 Receptor Antagonists. Receptor, Angiotensin, Type 2/antagonists ... Receptors, Adenosine A2/agonists. ... Receptor, Adenosine A2A/antagonists & inhibitors. Adenosine A2 ... Adenosine A2 Receptor Agonists. Receptor, Adenosine A2B/antagonists & inhibitors. Adenosine A2 Receptor Antagonists ...
... antagonists of the adenosine A2 receptors that complex with D2 receptors of the indirect striatopallidal pathway ameliorate ... Adenosine A1 receptor agonists impair the efficiency of the dopamine D1 receptors which could have implications for ... Administration of low doses of D2 receptor antagonist can stimulate pre-synaptic receptors leading to decreased locomotor ... Dopamine receptors belong to the 7 transmembrane, G protein-coupled receptor family (GPCRs). There are five receptor subtypes, ...
The aim of the present study was to examine the effects of adenosine A1 /A2 receptor activation on reperfusion-induced small ... A2 agonist, 0.1 mg/kg, i.v.)-treated I/R, and theophylline (non-selective A1 /A2 antagonist, 20 mg/kg, i.v.)-treated I/R groups ... Conclusion: We offer additional evidence that activation of A1 /A2 adenosine receptors provides partial protection against ... Objectives: Adenosine and adenosine A1 receptor agonists exert protective effects against reperfusion injury in different ...
... cell-surface A1 and A2 adenosine receptors). Although the exact mechanism by which adenosine receptor activation relaxes ... The vasoactive effects of adenosine are inhibited by adenosine receptor antagonists, (such as methylxanthines (e.g., caffeine, ... Methylxanthines, such as caffeine, aminophylline, and theophylline, are competitive adenosine receptor antagonists and ... adenosine is rapidly phosphorylated by adenosine kinase to adenosine monophosphate, or deaminated by adenosine deaminase to ...
Compounds that selectively bind to and activate ADENOSINE A2 RECEPTORS. HN - 2011 MH - Adenosine A2 Receptor Antagonists UI - ... ADENOSINE A2 RECEPTORS. HN - 2011 MH - Adenosine A3 Receptor Agonists UI - D058909 MN - D27.505.519.625.725.200.100.300 MN - ... Compounds that bind to and block the stimulation of ADENOSINE A1 RECEPTORS. HN - 2011 MH - Adenosine A2 Receptor Agonists UI - ... Compounds that bind to and stimulate ADENOSINE A1 RECEPTORS. HN - 2011 MH - Adenosine A1 Receptor Antagonists UI - D058916 MN ...
Coddou et al (2019) Characterization of the antagonist actions of 5-BDBD at the rat P2X4 receptor. Neurosci Lett 690 219 PMID: ... Dowd et al (1998) Adenosine A1 receptor-mediated excitation of nociceptive afferents innervating the normal and arthritic rat ... increase in vasomotion of guinea-pig mesenteric lymphatics involves an endothelium-dependent release of thromboxane A2. Br J ... P2 Receptors Scientific Review. Our Purine Receptor review gives an overview of the subtypes and structures of the P2 receptor ...
Comparative pharmacological studies on the A2 adenosine receptor agonist 5-n-ethyl-carboxamidoadenosine and its F19 isotope ... Investigation of the role of the serotonergic activity of certain subtype-selective alpha1A antagonists in the relaxant effect ... AT2 receptors and angiotensin II-mediated contractions of gastrointestinal tract of rats. Trakia Journal of Sciences, Vol. 10, ... Modulation of adenosine-induced responses in the guinea-pig trachea during long-term caffeine treatment: possible role of ...
3H]ZM241385-an antagonist radioligand for adenosine A2A receptors in rat brain European Journal of Pharmacology. 411(3), 205- ... A1 and A2 adenosine receptor modulation of contractility in the cauda epididymis of the guinea-pig. British Journal of ... A comparison of A2 adenosine receptor-induced cyclic AMP generation in cerebral cortex and relaxation of pre-contracted aorta. ... In vitro and in vivo effects of the A(2A) adenosine receptor antagonist KW-6002 on rat dopaminergic systems In: Summer Meeting ...
Warfarin and glycoprotein IIb/IIIa receptor antagonists There are no safety data from clinical trials as patients on warfarin ... Important platelet agonists in vivo, including thrombin, adenosine diphosphate, thromboxane A2 and collagen, all act via ... Oral glycoprotein IIb/IIIa receptor antagonists have been associated with a significant increase in mortality and higher rates ... Platelet glycoprotein IIb/IIIa receptor antagonists. In early studies, patients receiving abciximab had higher bleeding rates ...
Activation of adenosine A2A receptor promotes stellate cell collagen production. Adenosine release was increased in the liver ... Evaluating the role of cannabinoid receptor agonists and antagonists in the suppression of liver fibrosis ... A2 A receptor deficient mice were protected from development of hepatic fibrosis following exposure to CCl4 or thioacetamide. ... Adenosine:. Adenosine, a potent endogenous regulator of inflammation and tissue repair, is released in vitro by HepG2 cells in ...
... an A1 and A2 receptor antagonist used therapeutically to mitigate breathing problems in premature infants (Stevenson, 2007). ... Sichardt K, Nieber K (2007) Adenosine A(1) receptor: functional receptor-receptor interactions in the brain. Purinergic Signal ... suggesting blockade of A1 receptors did not reveal roles for A2 or A3 receptors that were otherwise masked by A1 receptor ... to activate adenosine receptors; 8-phenyltheophylline (8PT; 10 μM) to non-selectively block adenosine receptors; 8-cyclopentyl- ...
A3 Adenosine Receptor Antagonists (U.S. Patent Number 6,376,521). This invention relates to a method of decreasing intraocular ... Inverse agonists and neutral antagonists for the tsh receptor (U.S. Patent Application Number WO 2011127388 A2). ... Disclosed are A3 adenosine receptor antagonists and/or partial agonists of formula (I): wherein R1 to R5 are as described ... A3 Adenosine Receptor Antagonists and Partial Agonists (U.S. Patent Application Number 13/056,997). ...
... cell-surface A1 and A2 adenosine receptors). Although the exact mechanism by which adenosine receptor activation relaxes ... The vasoactive effects of adenosine are inhibited by adenosine receptor antagonists, (such as methylxanthines (e.g., caffeine, ... Methylxanthines, such as caffeine, aminophylline, and theophylline, are competitive adenosine receptor antagonists and ... adenosine is rapidly phosphorylated by adenosine kinase to adenosine monophosphate, or deaminated by adenosine deaminase to ...
Neutrophil adherence to endothelium is enhanced via adenosine A1 receptors and inhibited via adenosine A2 receptors. J Immunol ... Neugebauer V , Lücke T, Schaible HG.N-methyl-d-aspartate (NMDA) and non-NMDA receptor antagonists block the hyperexcitability ... activation by noradrenaline and adenosine of β adrenoreceptors and A2 adenosine receptors, respectively, inhibits inflammatory ... Indeed, systemic administration of the NMDA receptor antagonist, MK-801, was found to partially reduce the tactile allodynia ...
... an adenosine A1-receptor antagonist, but not 3,7-dimethyl-l-propargylxanthine (DMPX 1 mg/kg, ip), an adenosine A2A-receptor ... adenosine. thermal hyperalgesia. adenosine A1-receptors. formalin. adenosine A2-receptors. Issue Date: Jul-2008. ... Protective effect of adenosine in diabetic neuropathic pain is mediated through adenosine A1-receptors. ... Protective effect of adenosine in diabetic neuropathic pain is mediated through adenosine A1-receptors. Indian Journal of ...
Selectively blocks beta-1 receptors with little or no effect on beta-2 receptors. Is hydrophilic and does not penetrate CNS. ... Role of adenosine in pathogenesis of anginal pain. Circulation. 1990 Jan. 81(1):164-72. [QxMD MEDLINE Link]. ... Ranolazine elicits action unlike beta-blockers, calcium antagonists, or nitrates. It does not affect hemodynamics or ... Prevents platelet aggregation by irreversible cyclooxygenase inhibition with subsequent suppression of thromboxane A2. ...
... adenosine triphosphate, adenosine diphosphate (ADP), and serotonin).10 Platelets also synthesize and release thromboxane A2 ( ... adenosine triphosphate; ESKD, end-stage kidney disease; NO, nitric oxide; PAR, protease-activated receptor; TXA2, thromboxane 2 ... Use of vitamin K antagonists 1. ,. 42. Identified inherited/acquired thrombophilic factor 21. ,. 43. Postoperative heparin ... ADP, adenosine diphosphate; APC, activated protein C; ATP, adenosine triphosphate; CRP, C-reactive protein; FDP, fibrin ...
Wiethuchter, C. F., Lepe, V., Opazo, Á., Luzio, Á., Troncoso, I. & Hernandez, C., 1 Jan 2018, In: Revista de Investigaciones ... Fischer Wiethuchter, C., Toro, T. I., Luzio, Á., Opazo, Á., Carolina, R., Partarrieu Parra, J. & Cherres Villarroel, M., 1 Nov ... Lecea, B., Martínez, E., Aulí, M., Opazo, Á. & Clavé, P., 1 Dec 2009, In: Neurogastroenterology and Motility. 21, 12. Research ... Chávez, G. A. & Opazo, Á. J., 1 Nov 2012, In: Journal of Veterinary Behavior: Clinical Applications and Research. 7, 6, p. 386- ...

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