Interleukin-1beta: An interleukin-1 subtype that is synthesized as an inactive membrane-bound pro-protein. Proteolytic processing of the precursor form by CASPASE 1 results in release of the active form of interleukin-1beta from the membrane.Hormone Antagonists: 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.beta 2-Microglobulin: An 11-kDa protein associated with the outer membrane of many cells including lymphocytes. It is the small subunit of the MHC class I molecule. Association with beta 2-microglobulin is generally required for the transport of class I heavy chains from the endoplasmic reticulum to the cell surface. Beta 2-microglobulin is present in small amounts in serum, csf, and urine of normal people, and to a much greater degree in the urine and plasma of patients with tubular proteinemia, renal failure, or kidney transplants.Dopamine Antagonists: 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.Receptors, Adrenergic, beta: One of two major pharmacologically defined classes of adrenergic receptors. The beta adrenergic receptors play an important role in regulating CARDIAC MUSCLE contraction, SMOOTH MUSCLE relaxation, and GLYCOGENOLYSIS.Excitatory Amino Acid Antagonists: Drugs that bind to but do not activate excitatory amino acid receptors, thereby blocking the actions of agonists.Neurokinin-1 Receptor Antagonists: Compounds that inhibit or block the activity of NEUROKININ-1 RECEPTORS.Interleukin 1 Receptor Antagonist Protein: 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.Narcotic Antagonists: Agents inhibiting the effect of narcotics on the central nervous system.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Histamine H2 Antagonists: 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.Muscarinic Antagonists: 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.Integrin beta3: An integrin beta subunit of approximately 85-kDa in size which has been found in INTEGRIN ALPHAIIB-containing and INTEGRIN ALPHAV-containing heterodimers. Integrin beta3 occurs as three alternatively spliced isoforms, designated beta3A-C.Rats, Sprague-Dawley: A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.GABA Antagonists: Drugs that bind to but do not activate GABA RECEPTORS, thereby blocking the actions of endogenous GAMMA-AMINOBUTYRIC ACID and GABA RECEPTOR AGONISTS.Nicotinic Antagonists: 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.Histamine H1 Antagonists: 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.Piperidines: A family of hexahydropyridines.Purinergic P1 Receptor Antagonists: Compounds that bind to and block the stimulation of PURINERGIC P1 RECEPTORS.Histamine Antagonists: 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.Cells, Cultured: Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.Transforming Growth Factor beta: A factor synthesized in a wide variety of tissues. It acts synergistically with TGF-alpha in inducing phenotypic transformation and can also act as a negative autocrine growth factor. TGF-beta has a potential role in embryonal development, cellular differentiation, hormone secretion, and immune function. TGF-beta is found mostly as homodimer forms of separate gene products TGF-beta1, TGF-beta2 or TGF-beta3. Heterodimers composed of TGF-beta1 and 2 (TGF-beta1.2) or of TGF-beta2 and 3 (TGF-beta2.3) have been isolated. The TGF-beta proteins are synthesized as precursor proteins.Adenosine A2 Receptor Antagonists: Compounds that selectively bind to and block the activation of ADENOSINE A2 RECEPTORS.Purinergic P2 Receptor Antagonists: Compounds that bind to and block the stimulation of PURINERGIC P2 RECEPTORS.Adrenergic alpha-1 Receptor Antagonists: Drugs that bind to and block the activation of ADRENERGIC ALPHA-1 RECEPTORS.Serotonin 5-HT3 Receptor Antagonists: Drugs that bind to but do not activate SEROTONIN 5-HT3 RECEPTORS, thereby blocking the actions of SEROTONIN or SEROTONIN 5-HT3 RECEPTOR AGONISTS.Rats, Wistar: A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.Serotonin 5-HT2 Receptor Antagonists: 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.Signal Transduction: The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.Adenosine A1 Receptor Antagonists: Compounds that bind to and block the stimulation of ADENOSINE A1 RECEPTORS.Leukotriene Antagonists: A class of drugs designed to prevent leukotriene synthesis or activity by blocking binding at the receptor level.Cell Line: Established cell cultures that have the potential to propagate indefinitely.RNA, Messenger: 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.Angiotensin Receptor Antagonists: Agents that antagonize ANGIOTENSIN RECEPTORS. Many drugs in this class specifically target the ANGIOTENSIN TYPE 1 RECEPTOR.Adrenergic Antagonists: Drugs that bind to but do not activate ADRENERGIC RECEPTORS. Adrenergic antagonists block the actions of the endogenous adrenergic transmitters EPINEPHRINE and NOREPINEPHRINE.Interleukin-1: 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.Receptors, Adrenergic, beta-2: A subclass of beta-adrenergic receptors (RECEPTORS, ADRENERGIC, BETA). The adrenergic beta-2 receptors are more sensitive to EPINEPHRINE than to NOREPINEPHRINE and have a high affinity for the agonist TERBUTALINE. They are widespread, with clinically important roles in SKELETAL MUSCLE; LIVER; and vascular, bronchial, gastrointestinal, and genitourinary SMOOTH MUSCLE.Integrin alpha5beta1: An integrin found in FIBROBLASTS; PLATELETS; MONOCYTES, and LYMPHOCYTES. Integrin alpha5beta1 is the classical receptor for FIBRONECTIN, but it also functions as a receptor for LAMININ and several other EXTRACELLULAR MATRIX PROTEINS.GABA-A Receptor Antagonists: Drugs that bind to but do not activate GABA-A RECEPTORS thereby blocking the actions of endogenous or exogenous GABA-A RECEPTOR AGONISTS.Binding, Competitive: 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.Adrenergic alpha-2 Receptor Antagonists: Drugs that bind to and block the activation of ADRENERGIC ALPHA-2 RECEPTORS.Radioligand Assay: Quantitative determination of receptor (binding) proteins in body fluids or tissue using radioactively labeled binding reagents (e.g., antibodies, intracellular receptors, plasma binders).Integrin beta4: Also known as CD104 antigen, this protein is distinguished from other beta integrins by its relatively long cytoplasmic domain (approximately 1000 amino acids vs. approximately 50). Five alternatively spliced isoforms have been described.Adrenergic beta-Antagonists: Drugs that bind to but do not activate beta-adrenergic receptors thereby blocking the actions of beta-adrenergic agonists. Adrenergic beta-antagonists are used for treatment of hypertension, cardiac arrhythmias, angina pectoris, glaucoma, migraine headaches, and anxiety.Adrenergic alpha-Antagonists: 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.Integrin alpha6beta4: This intrgrin is a key component of HEMIDESMOSOMES and is required for their formation and maintenance in epithelial cells. Integrin alpha6beta4 is also found on thymocytes, fibroblasts, and Schwann cells, where it functions as a laminin receptor (RECEPTORS, LAMININ) and is involved in wound healing, cell migration, and tumor invasiveness.Integrin alpha4beta1: Integrin alpha4beta1 is a FIBRONECTIN and VCAM-1 receptor present on LYMPHOCYTES; MONOCYTES; EOSINOPHILS; NK CELLS and thymocytes. It is involved in both cell-cell and cell- EXTRACELLULAR MATRIX adhesion and plays a role in INFLAMMATION, hematopoietic cell homing and immune function, and has been implicated in skeletal MYOGENESIS; NEURAL CREST migration and proliferation, lymphocyte maturation and morphogenesis of the PLACENTA and HEART.Integrin beta Chains: Integrin beta chains combine with integrin alpha chains to form heterodimeric cell surface receptors. Integrins have traditionally been classified into functional groups based on the identity of one of three beta chains present in the heterodimer. The beta chain is necessary and sufficient for integrin-dependent signaling. Its short cytoplasmic tail contains sequences critical for inside-out signaling.beta 2-Glycoprotein I: A 44-kDa highly glycosylated plasma protein that binds phospholipids including CARDIOLIPIN; APOLIPOPROTEIN E RECEPTOR; membrane phospholipids, and other anionic phospholipid-containing moieties. It plays a role in coagulation and apoptotic processes. Formerly known as apolipoprotein H, it is an autoantigen in patients with ANTIPHOSPHOLIPID ANTIBODIES.Propanolamines: AMINO ALCOHOLS containing the propanolamine (NH2CH2CHOHCH2) group and its derivatives.Histamine H3 Antagonists: Drugs that selectively bind to but do not activate HISTAMINE H3 RECEPTORS. They have been used to correct SLEEP WAKE DISORDERS and MEMORY DISORDERS.Receptors, Adrenergic, beta-1: A subclass of beta-adrenergic receptors (RECEPTORS, ADRENERGIC, BETA). The adrenergic beta-1 receptors are equally sensitive to EPINEPHRINE and NOREPINEPHRINE and bind the agonist DOBUTAMINE and the antagonist METOPROLOL with high affinity. They are found in the HEART, juxtaglomerular cells, and in the central and peripheral nervous systems.Pyridines: Compounds with a six membered aromatic ring containing NITROGEN. The saturated version is PIPERIDINES.Integrin alpha2beta1: An integrin found on fibroblasts, platelets, endothelial and epithelial cells, and lymphocytes where it functions as a receptor for COLLAGEN and LAMININ. Although originally referred to as the collagen receptor, it is one of several receptors for collagen. Ligand binding to integrin alpha2beta1 triggers a cascade of intracellular signaling, including activation of p38 MAP kinase.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Adrenergic beta-Agonists: Drugs that selectively bind to and activate beta-adrenergic receptors.Ligands: A molecule that binds to another molecule, used especially to refer to a small molecule that binds specifically to a larger molecule, e.g., an antigen binding to an antibody, a hormone or neurotransmitter binding to a receptor, or a substrate or allosteric effector binding to an enzyme. Ligands are also molecules that donate or accept a pair of electrons to form a coordinate covalent bond with the central metal atom of a coordination complex. (From Dorland, 27th ed)Receptors, Serotonin: 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.Mice, Inbred C57BLReceptors, Endothelin: Cell surface proteins that bind ENDOTHELINS with high affinity and trigger intracellular changes which influence the behavior of cells.Guinea Pigs: A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.Kinetics: The rate dynamics in chemical or physical systems.Adrenergic beta-2 Receptor Antagonists: Drugs that bind to and block the activation of ADRENERGIC BETA-2 RECEPTORS.Calcium Channel Blockers: A class of drugs that act by selective inhibition of calcium influx through cellular membranes.Receptors, N-Methyl-D-Aspartate: 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.Oligopeptides: Peptides composed of between two and twelve amino acids.Recombinant Proteins: Proteins prepared by recombinant DNA technology.Integrins: A family of transmembrane glycoproteins (MEMBRANE GLYCOPROTEINS) consisting of noncovalent heterodimers. They interact with a wide variety of ligands including EXTRACELLULAR MATRIX PROTEINS; COMPLEMENT, and other cells, while their intracellular domains interact with the CYTOSKELETON. The integrins consist of at least three identified families: the cytoadhesin receptors(RECEPTORS, CYTOADHESIN), the leukocyte adhesion receptors (RECEPTORS, LEUKOCYTE ADHESION), and the VERY LATE ANTIGEN RECEPTORS. Each family contains a common beta-subunit (INTEGRIN BETA CHAINS) combined with one or more distinct alpha-subunits (INTEGRIN ALPHA CHAINS). These receptors participate in cell-matrix and cell-cell adhesion in many physiologically important processes, including embryological development; HEMOSTASIS; THROMBOSIS; WOUND HEALING; immune and nonimmune defense mechanisms; and oncogenic transformation.Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.Serotonin 5-HT1 Receptor Antagonists: 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.Binding Sites: The parts of a macromolecule that directly participate in its specific combination with another molecule.Dizocilpine Maleate: 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.Neurons: 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.Peptide Fragments: Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.Drug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug.Estrogen Antagonists: Compounds which inhibit or antagonize the action or biosynthesis of estrogenic compounds.Indoles: 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.Benzazepines: Compounds with BENZENE fused to AZEPINES.Antigens, CD29: Integrin beta-1 chains which are expressed as heterodimers that are noncovalently associated with specific alpha-chains of the CD49 family (CD49a-f). CD29 is expressed on resting and activated leukocytes and is a marker for all of the very late activation antigens on cells. (from: Barclay et al., The Leukocyte Antigen FactsBook, 1993, p164)Biphenyl CompoundsCricetinae: A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.Adenosine A3 Receptor Antagonists: Compounds that selectively bind to and block the activation of ADENOSINE A3 RECEPTORS.Sulfonamides: A group of compounds that contain the structure SO2NH2.Sialoglycoproteins: 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.Receptors, Adrenergic, beta-3: A subclass of beta-adrenergic receptors (RECEPTORS, ADRENERGIC, BETA). The beta-3 adrenergic receptors are the predominant beta-adrenergic receptor type expressed in white and brown ADIPOCYTES and are involved in modulating ENERGY METABOLISM and THERMOGENESIS.CHO Cells: CELL LINE derived from the ovary of the Chinese hamster, Cricetulus griseus (CRICETULUS). The species is a favorite for cytogenetic studies because of its small chromosome number. The cell line has provided model systems for the study of genetic alterations in cultured mammalian cells.Receptor, Endothelin A: A subtype of endothelin receptor found predominantly in the VASCULAR SMOOTH MUSCLE. It has a high affinity for ENDOTHELIN-1 and ENDOTHELIN-2.Integrin alpha6beta1: A cell surface receptor mediating cell adhesion to the EXTRACELLULAR MATRIX and to other cells via binding to LAMININ. It is involved in cell migration, embryonic development, leukocyte activation and tumor cell invasiveness. Integrin alpha6beta1 is the major laminin receptor on PLATELETS; LEUKOCYTES; and many EPITHELIAL CELLS, and ligand binding may activate a number of signal transduction pathways. Alternative splicing of the cytoplasmic domain of the alpha6 subunit (INTEGRIN ALPHA6) results in the formation of A and B isoforms of the heterodimer, which are expressed in a tissue-specific manner.Base Sequence: The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.Estrogen Receptor beta: One of the ESTROGEN RECEPTORS that has greater affinity for ISOFLAVONES than ESTROGEN RECEPTOR ALPHA does. There is great sequence homology with ER alpha in the DNA-binding domain but not in the ligand binding and hinge domains.Peptides, Cyclic: 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).PiperazinesNaltrexone: 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.Mice, Knockout: Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.Transfection: The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.Receptors, Nicotinic: One of the two major classes of cholinergic receptors. Nicotinic receptors were originally distinguished by their preference for NICOTINE over MUSCARINE. They are generally divided into muscle-type and neuronal-type (previously ganglionic) based on pharmacology, and subunit composition of the receptors.Disease Models, Animal: 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.Pyrazoles: 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.Structure-Activity Relationship: The relationship between the chemical structure of a compound and its biological or pharmacological activity. Compounds are often classed together because they have structural characteristics in common including shape, size, stereochemical arrangement, and distribution of functional groups.Gene Expression Regulation: Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.Xanthines: Purine bases found in body tissues and fluids and in some plants.Purinergic P2X Receptor Antagonists: Compounds that bind to and block the stimulation of PURINERGIC P2X RECEPTORS. Included under this heading are antagonists for specific P2X receptor subtypes.Serotonin Receptor Agonists: 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.Substance P: 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.Naloxone: A specific opiate antagonist that has no agonist activity. It is a competitive antagonist at mu, delta, and kappa opioid receptors.Glycogen Synthase Kinase 3: A glycogen synthase kinase that was originally described as a key enzyme involved in glycogen metabolism. It regulates a diverse array of functions such as CELL DIVISION, microtubule function and APOPTOSIS.Azepines: Seven membered heterocyclic rings containing a NITROGEN atom.Integrin alpha1beta1: Integrin alpha1beta1 functions as a receptor for LAMININ and COLLAGEN. It is widely expressed during development, but in the adult is the predominant laminin receptor (RECEPTORS, LAMININ) in mature SMOOTH MUSCLE CELLS, where it is important for maintenance of the differentiated phenotype of these cells. Integrin alpha1beta1 is also found in LYMPHOCYTES and microvascular endothelial cells, and may play a role in angiogenesis. In SCHWANN CELLS and neural crest cells, it is involved in cell migration. Integrin alpha1beta1 is also known as VLA-1 and CD49a-CD29.Transforming Growth Factor beta1: A subtype of transforming growth factor beta that is synthesized by a wide variety of cells. It is synthesized as a precursor molecule that is cleaved to form mature TGF-beta 1 and TGF-beta1 latency-associated peptide. The association of the cleavage products results in the formation a latent protein which must be activated to bind its receptor. Defects in the gene that encodes TGF-beta1 are the cause of CAMURATI-ENGELMANN SYNDROME.Purinergic Antagonists: Drugs that bind to and block the activation of PURINERGIC RECEPTORS.Serotonin: 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.PyrrolidinesQuinoxalinesElectric Stimulation: Use of electric potential or currents to elicit biological responses.Behavior, Animal: The observable response an animal makes to any situation.Cell Adhesion: Adherence of cells to surfaces or to other cells.Norepinephrine: 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.Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.Adrenergic beta-2 Receptor Agonists: Compounds bind to and activate ADRENERGIC BETA-2 RECEPTORS.Prazosin: A selective adrenergic alpha-1 antagonist used in the treatment of HEART FAILURE; HYPERTENSION; PHEOCHROMOCYTOMA; RAYNAUD DISEASE; PROSTATIC HYPERTROPHY; and URINARY RETENTION.Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.TetrazolesCyclic AMP: An adenine nucleotide containing one phosphate group which is esterified to both the 3'- and 5'-positions of the sugar moiety. It is a second messenger and a key intracellular regulator, functioning as a mediator of activity for a number of hormones, including epinephrine, glucagon, and ACTH.Gene Expression: The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.Rabbits: The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.Cannabinoid Receptor Antagonists: Compounds that inhibit or block the activity of CANNABINOID RECEPTORS.Brain: 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.Receptors, Neurokinin-1: 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.Muscle Contraction: 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.Prostaglandin Antagonists: Compounds that inhibit the action of prostaglandins.Isoproterenol: Isopropyl analog of EPINEPHRINE; beta-sympathomimetic that acts on the heart, bronchi, skeletal muscle, alimentary tract, etc. It is used mainly as bronchodilator and heart stimulant.Receptors, Dopamine D2: 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.Dioxanes: 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)Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.Blotting, Western: Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.Adenosine: A nucleoside that is composed of ADENINE and D-RIBOSE. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter.Yohimbine: A plant alkaloid with alpha-2-adrenergic blocking activity. Yohimbine has been used as a mydriatic and in the treatment of ERECTILE DYSFUNCTION.Mineralocorticoid Receptor Antagonists: Drugs that bind to and block the activation of MINERALOCORTICOID RECEPTORS by MINERALOCORTICOIDS such as ALDOSTERONE.Reverse Transcriptase Polymerase Chain Reaction: A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.Injections, Intraventricular: Injections into the cerebral ventricles.Propranolol: A widely used non-cardioselective beta-adrenergic antagonist. Propranolol has been used for MYOCARDIAL INFARCTION; ARRHYTHMIA; ANGINA PECTORIS; HYPERTENSION; HYPERTHYROIDISM; MIGRAINE; PHEOCHROMOCYTOMA; and ANXIETY but adverse effects instigate replacement by newer drugs.Receptors, Opioid: 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.Muscle, Smooth: 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)GABA-B Receptor Antagonists: Drugs that bind to but do not activate GABA-B RECEPTORS thereby blocking the actions of endogenous or exogenous GABA-B RECEPTOR AGONISTS.Ketanserin: 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.Receptor, Cannabinoid, CB1: A subclass of cannabinoid receptor found primarily on central and peripheral NEURONS where it may play a role modulating NEUROTRANSMITTER release.Receptors, Vasopressin: 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.Blood Pressure: PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.beta Catenin: A multi-functional catenin that participates in CELL ADHESION and nuclear signaling. Beta catenin binds CADHERINS and helps link their cytoplasmic tails to the ACTIN in the CYTOSKELETON via ALPHA CATENIN. It also serves as a transcriptional co-activator and downstream component of WNT PROTEIN-mediated SIGNAL TRANSDUCTION PATHWAYS.Receptors, G-Protein-Coupled: The largest family of cell surface receptors involved in SIGNAL TRANSDUCTION. They share a common structure and signal through HETEROTRIMERIC G-PROTEINS.Tumor Necrosis Factor-alpha: Serum glycoprotein produced by activated MACROPHAGES and other mammalian MONONUCLEAR LEUKOCYTES. It has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. Also known as TNF-alpha, it is only 30% homologous to TNF-beta (LYMPHOTOXIN), but they share TNF RECEPTORS.Pindolol: A moderately lipophilic beta blocker (ADRENERGIC BETA-ANTAGONISTS). It is non-cardioselective and has intrinsic sympathomimetic actions, but little membrane-stabilizing activity. (From Martindale, The Extra Pharmocopoeia, 30th ed, p638)Receptors, Opioid, mu: 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.BenzodiazepinonesEndothelin-1: 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)Receptor, Endothelin B: A subtype of endothelin receptor found predominantly in the KIDNEY. It may play a role in reducing systemic ENDOTHELIN levels.Receptors, Cholecystokinin: 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.N-Methylaspartate: An amino acid that, as the D-isomer, is the defining agonist for the NMDA receptor subtype of glutamate receptors (RECEPTORS, NMDA).Tumor Cells, Cultured: Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents.Models, Molecular: Models used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.Cholinergic Antagonists: Drugs that bind to but do not activate CHOLINERGIC RECEPTORS, thereby blocking the actions of ACETYLCHOLINE or cholinergic agonists.Patch-Clamp Techniques: 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.Capsaicin: An alkylamide found in CAPSICUM that acts at TRPV CATION CHANNELS.Receptors, Bradykinin: 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.Bicuculline: An isoquinoline alkaloid obtained from Dicentra cucullaria and other plants. It is a competitive antagonist for GABA-A receptors.Receptors, GABA-A: Cell surface proteins which bind GAMMA-AMINOBUTYRIC ACID and contain an integral membrane chloride channel. Each receptor is assembled as a pentamer from a pool of at least 19 different possible subunits. The receptors belong to a superfamily that share a common CYSTEINE loop.Bradykinin: 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.Receptors, Purinergic P1: A class of cell surface receptors that prefer ADENOSINE to other endogenous PURINES. Purinergic P1 receptors are widespread in the body including the cardiovascular, respiratory, immune, and nervous systems. There are at least two pharmacologically distinguishable types (A1 and A2, or Ri and Ra).2-Amino-5-phosphonovalerate: 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.Gonadotropin-Releasing Hormone: A decapeptide that stimulates the synthesis and secretion of both pituitary gonadotropins, LUTEINIZING HORMONE and FOLLICLE STIMULATING HORMONE. GnRH is produced by neurons in the septum PREOPTIC AREA of the HYPOTHALAMUS and released into the pituitary portal blood, leading to stimulation of GONADOTROPHS in the ANTERIOR PITUITARY GLAND.Beta Rhythm: Brain waves with frequency between 15-30 Hz seen on EEG during wakefulness and mental activity.Losartan: An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.Receptors, Opioid, kappa: 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.Glutamic Acid: A non-essential amino acid naturally occurring in the L-form. Glutamic acid is the most common excitatory neurotransmitter in the CENTRAL NERVOUS SYSTEM.Receptors, Neurokinin-2: 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.Histamine: 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.Electrophysiology: 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.Bicyclo Compounds, Heterocyclic: A class of saturated compounds consisting of two rings only, having two or more atoms in common, containing at least one hetero atom, and that take the name of an open chain hydrocarbon containing the same total number of atoms. (From Riguady et al., Nomenclature of Organic Chemistry, 1979, p31)Benzimidazoles: Compounds with a BENZENE fused to IMIDAZOLES.Adrenergic beta-3 Receptor Antagonists: Drugs that bind to and block the activation of ADRENERGIC BETA-3 RECEPTORS.Adrenergic beta-1 Receptor Antagonists: Drugs that bind to and block the activation of ADRENERGIC BETA-1 RECEPTORS.Protein Subunits: Single chains of amino acids that are the units of multimeric PROTEINS. Multimeric proteins can be composed of identical or non-identical subunits. One or more monomeric subunits may compose a protomer which itself is a subunit structure of a larger assembly.Cell Membrane: The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.Receptors, Interleukin-1: 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.QuinolinesAdrenergic alpha-Agonists: Drugs that selectively bind to and activate alpha adrenergic receptors.Naphthalenes: 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.Acetylcholine: A neurotransmitter found at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system.Synaptic Transmission: 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.Cell Line, Tumor: A cell line derived from cultured tumor cells.Receptors, Muscarinic: One of the two major classes of cholinergic receptors. Muscarinic receptors were originally defined by their preference for MUSCARINE over NICOTINE. There are several subtypes (usually M1, M2, M3....) that are characterized by their cellular actions, pharmacology, and molecular biology.Cytokines: Non-antibody proteins secreted by inflammatory leukocytes and some non-leukocytic cells, that act as intercellular mediators. They differ from classical hormones in that they are produced by a number of tissue or cell types rather than by specialized glands. They generally act locally in a paracrine or autocrine rather than endocrine manner.Dogs: The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)QuinuclidinesAngiotensin II: 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.gamma-Aminobutyric Acid: The most common inhibitory neurotransmitter in the central nervous system.Rats, Inbred Strains: Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.Protein Conformation: The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. PROTEIN STRUCTURE, QUATERNARY describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain).DNA Polymerase beta: A DNA repair enzyme that catalyzes DNA synthesis during base excision DNA repair. EC 2.7.7.7.
(1/4656) Cardiac sympathetic activity estimated by 123I-MIBG myocardial imaging in patients with dilated cardiomyopathy after beta-blocker or angiotensin-converting enzyme inhibitor therapy.

Impaired cardiac sympathetic activity can be evaluated by 123I-metaiodobenzylguanidine (MIBG) imaging. METHODS: We studied the significance of MIBG imaging for 24 patients (age 58+/-12 y) with dilated cardiomyopathy (DCM). We compared 12 patients (group A) treated with metoprolol (dose from 30-60 mg/d) with 12 patients treated with angiotensin-converting enzyme (ACE) inhibitors. Patients were studied before treatment, after 5 mo of treatment (only in group A) and after 1 y of treatment. Cardiac MIBG uptake was assessed as the heart-to-mediastinum activity ratio (H/M) and total defect score (TDS) from anterior planar and SPECT MIBG images, which were acquired in 4 h after tracer injection. New York Heart Association (NYHA) class and left ventricular ejection fraction (LVEF) calculated by echocardiography were also assessed. RESULTS: TDS decreased in both groups (in group A, from 30+/-7 through 23+/-9 to 18+/-10; P < 0.01, in group B, from 30+/-6 to 24+/-8; P < 0.01) and H/M was increased in both groups (in group A, from 1.87+/-0.31 through 2.03+/-0.28 to 2.14+/-0.29; P < 0.01, in group B, from 1.82+/-0.28 to 1.94+/-0.26; P < 0.05). But TDS and H/M were more improved in group A than in group B (P < 0.05). LVEF was significantly increased in only group A (from 38+/-6 through 43+/-8 to 49%+/-9%; P < 0.01). NYHA improved in both groups (in group A, from mean 2.5 through 2.1 to 1.8; P < 0.01, in group B, from mean 2.6 to 2.1; P < 0.05) but was more improved in group A than in group B (P < 0.05). CONCLUSION: Cardiac function, symptom and cardiac sympathetic activity evaluated by MIBG images improved after the beta-blocker therapy more than with the treatment that used ACE inhibitors.  (+info)

(2/4656) Sympathetic nerve alterations assessed with 123I-MIBG in the failing human heart.

Norepinephrine (NE) reuptake function is impaired in heart failure and this may participate in myocyte hyperstimulation by the neurotransmitter. This alteration can be assessed by 123I-metaiodobenzylguanidine (MIBG) scintigraphy. METHODS: To determine whether the impairment of neuronal NE reuptake was reversible after metoprolol therapy, we studied 18 patients (43+/-7 y) with idiopathic dilated cardiomyopathy who were stabilized at least for 3 mo with captopril and diuretics. Patients underwent, before and after 6 mo of therapy with metoprolol, measurements of radionuclide left ventricular ejection fraction (LVEF), maximal oxygen consumption and plasma NE concentration. The cardiac adrenergic innervation function was scintigraphically assessed with MIBG uptake and release measurements on the planar images obtained 20 min and 4 h after tracer injection. To evaluate whether metoprolol had a direct interaction with cardiac MIBG uptake and release, six normal subjects were studied before and after a 1-mo metoprolol intake. RESULTS: In controls, neither cardiac MIBG uptake and release nor circulating NE concentration changed after the 1-mo metoprolol intake. Conversely, after a 6-mo therapy with metoprolol, patients showed increased cardiac MIBG uptake (129%+/-10% versus 138%+/-17%; P = 0.009), unchanged cardiac MIBG release and decreased plasma NE concentration (0.930+/-412 versus 0.721+/-0.370 ng/mL; P = 0.02). In parallel, patients showed improved New York Heart Association class (2.44+/-0.51 versus 2.05+/-0.23; P = 0.004) and increased LVEF (20%+/-8% versus 27%+/-8%; P = 0.0005), whereas maximal oxygen uptake remained unchanged. CONCLUSION: Thus, a parallel improvement of myocardial NE reuptake and of hemodynamics was observed after a 6-mo metoprolol therapy, suggesting that such agents may be beneficial in heart failure by directly protecting the myocardium against excessive NE stimulation.  (+info)

(3/4656) QT dispersion in patients with chronic heart failure: beta blockers are associated with a reduction in QT dispersion.

OBJECTIVE: To compare QT dispersion in patients with impaired left ventricular systolic function and in matched control patients with normal left ventricular systolic function. DESIGN: A retrospective, case-control study with controls matched 4:1 for age, sex, previous myocardial infarction, and diuretic and beta blocker treatment. SETTING: A regional cardiology centre and a university teaching hospital. PATIENTS: 25 patients with impaired left ventricular systolic function and 100 patients with normal left ventricular systolic function. MAIN OUTCOME MEASURES: QT and QTc dispersion measured by three methods: the difference between maximum and minimum QT and QTc intervals, the standard deviation of QT and QTc intervals, and the "lead adjusted" QT and QTc dispersion. RESULTS: All measures of QT/QTc dispersion were closely interrelated (r values 0.86 to 0.99; all p < 0.001). All measures of QT and QTc dispersion were significantly increased in the patients with impaired left ventricular systolic function v controls (p < 0.001): 71.9 (6.5) (mean (SEM)) v 46.9 (1.7) ms for QT dispersion, and 83.6 (7.6) v 54.3 (2.1) ms(-1-2) for QTc dispersion. All six dispersion parameters were reduced in patients taking beta blockers (p < 0.05), regardless of whether left ventricular function was normal or impaired-by 9.4 (4.6) ms for QT dispersion (p < 0.05) and by 13.8 (6. 5) ms(-1-2) for QTc dispersion (p = 0.01). CONCLUSIONS: QT and QTc dispersion are increased in patients with systolic heart failure in comparison with matched controls, regardless of the method of measurement and independently of possible confounding factors. beta Blockers are associated with a reduction in both QT and QTc dispersion, raising the possibility that a reduction in dispersion of ventricular repolarisation may be an important antiarrhythmic mechanism of beta blockade.  (+info)

(4/4656) AV reentrant and idiopathic ventricular double tachycardias: complicated interactions between two tachycardias.

An electrophysiological study was performed in a 61 year old man with Wolff- Parkinson-White (WPW) syndrome. At baseline, neither ventricular nor supraventricular tachycardias could be induced. During isoprenaline infusion, ventricular tachycardia originating from the right ventricular outflow tract (RVOT) with a cycle length of 280 ms was induced and subsequently atrioventricular reentrant tachycardia (AVRT) with a cycle length of 300 ms using an accessory pathway in the left free wall appeared. During these tachycardias, AVRT was entrained by ventricular tachycardia. The earliest ventricular activation site during the ventricular tachycardia was determined to be the RVOT site and a radiofrequency current at 30 W successfully ablated the ventricular tachycardia at this site. The left free wall accessory pathway was also successfully ablated during right ventricular pacing. The coexistence of WPW syndrome and cathecolamine sensitive ventricular tachycardia originating from the RVOT has rarely been reported. Furthermore, the tachycardias were triggered by previous tachycardias.  (+info)

(5/4656) Kinetic analysis of drug-receptor interactions of long-acting beta2 sympathomimetics in isolated receptor membranes: evidence against prolonged effects of salmeterol and formoterol on receptor-coupled adenylyl cyclase.

The long-acting beta2 sympathomimetics salmeterol and formoterol have been presumed to exert their prolonged action either by binding to an accessory binding site ("exo-site") near the beta2 adrenoceptor or by their high affinity for beta2 adrenoceptors and correspondingly slow dissociation. Whereas most studies with salmeterol had been done in intact tissues, which have slow diffusion and compartmentation of drugs in lipophilic phases, that restrict drug access to the receptor biophase, we used purified receptor membranes from rat lung and disaggregated calf tracheal myocytes as model systems. Binding experiments were designed to measure the slow dissociation of agonists by means of delayed association of (-)-[125I]iodopindolol. Rat lung membranes were pretreated with high concentrations of agonists (salmeterol, formoterol, isoprenaline) before dissociation was induced by 50-fold dilution. Half-times of association of (-)-[125I]iodopindolol remained unchanged compared with untreated controls, indicating that dissociation of agonists occurred in less than 2 min. Adenylyl cyclase experiments were designed to determine the on and off kinetics of agonists to beta2 adrenoceptors by measuring the rate of receptor-induced cyclic AMP (cAMP) formation. Experiments were performed in tracheal membranes characterized by high Vmax values of cAMP formation. Adenylyl cyclase activation occurred simultaneously with the addition of the agonist, continued linearly with time for 60 min, and ceased immediately after the antagonist was added. Similarly, when receptor membranes were preincubated in a small volume with high salmeterol concentrations, there was a linear increase in cAMP formation, which was immediately interrupted by a 100-fold dilution of the reaction mixture. This militates against the exo-site hypothesis. On the other hand, dissociation by dilution was much less when membranes were preincubated with a large volume of salmeterol at the same concentration, indicating that physicochemical effects, and not exo-site binding, underlie its prolonged mode of action.  (+info)

(6/4656) Mechanisms of prostaglandin E2 release by intact cells expressing cyclooxygenase-2: evidence for a 'two-component' model.

Prostaglandin (PG) release in cells expressing constitutive cyclooxygenase-1 is known to be regulated by liberation of arachidonic acid by phospholipase A2 followed by metabolism by cyclooxygenase. However, the relative contribution of phospholipase A2 to the release of PGs in cells expressing cyclooxygenase-2 is not clear. We addressed this question by using radioimmunoassay to measure PGE2 release by human cells (A549) induced to express cyclooxygenase-2 (measured by Western blot analysis) by interleukin-1beta. Cells were either unstimulated or stimulated with agents known to activate phospholipase A2 (bradykinin, Des-Arg10-kallidin, or the calcium ionophore A23187) or treated with exogenous arachidonic acid. When cells were treated to express cyclooxygenase-2, the levels of PGE2 released over 15 min were undetectable; however, in the same cells stimulated with bradykinin, A23187, or arachidonic acid, large amounts of prostanoid were produced. Using selective inhibitors/antagonists, we found that the effects of bradykinin were mediated by B2 receptor activation and that prostanoid release was due to cyclooxygenase-2, and not cyclooxygenase-1, activity. In addition, we show that the release of PGE2 stimulated by either bradykinin, A23187, or arachidonic acid was inhibited by the phospholipase A2 inhibitor arachidonate trifluoromethyl ketone. Hence, we have demonstrated that PGE2 is released by two components: induction of cyclooxygenase-2 and supply of substrate, probably via activation of phospholipase A2. This is illustrated in A549 cells by a clear synergy between the cytokine interleukin-1beta and the kinin bradykinin.  (+info)

(7/4656) Evidence for beta3-adrenoceptor subtypes in relaxation of the human urinary bladder detrusor: analysis by molecular biological and pharmacological methods.

The purpose of the present study was to confirm the presence of beta3-adrenoceptor subtype in the relaxation of human urinary bladder detrusor tissue by reverse transcription-polymerase chain reaction (PCR); direct sequencing of the PCR product, in situ hybridization; and isometric contraction. Using reverse transcription-PCR, the mRNAs of three receptor subtypes (beta1, beta2, and beta3) were expressed in the human urinary bladder detrusor tissue. Direct sequencing of the PCR product of the above beta3-adrenoceptor revealed no mutation in the amplified regions. In situ hybridization with digoxygenin-labeled oligonucleotide probe revealed the presence of the mRNA of beta3-adrenoceptor subtype in the smooth muscle of the urinary bladder. The relaxant effects of isoproterenol (a nonselective beta-adrenoceptor agonist); ZD7114, BRL37344, and CGP12177A (putative selective beta3-adrenoceptor agonists); and SR59230A (a putative selective beta3-adrenoceptor antagonist) were tested using an isometric contraction technique. Isoproterenol in either the presence or absence of both atenolol (a beta1-adrenoceptor-selective antagonist) and butoxamine (a beta2-adrenoceptor-selective antagonist) revealed a relaxant effect on the carbachol-induced contraction of the human urinary bladder detrusor. Both BRL37344 and CGP12177A also revealed relaxant effects on the human urinary bladder detrusor, but ZD7114 did not elicit any relaxation. These results suggest that beta3-adrenoceptor may have some role in urine storage in the human urinary bladder.  (+info)

(8/4656) Adrenoreceptors of the guinea-pig urinary bladder.

1 Adrenaline, noradrenaline and isoprenaline (5 mug/ml) did not affect the resting tone of the isolated urinary bladder of the guinea-pig. 2 The catecholamines (1-2 mug/ml) inhibited neuronally evoked contractions at various stimulation frequencies; the inhibition was maximum at 2 Hz and minimum at 50 Hz. Isoprenaline produced maximum inhibition. 3 Propranolol (0.5 mug/ml) completely blocked the catecholamine-induced inhibition at all the frequencies employed. The concentration-response curves of isoprenaline at 2, 10 and 50 Hz were characteristically shifted by propranolol (50 ng/ml). Phenoxybenzamine (0.2 mug/ml) was totally ineffective. 4 In some experiments adrenaline significantly raised the tone of the bladder exposed to propranolol; this effect could be blocked by phenoxybenzamine. 5 Acetylcholine-induced bladder contractions were inhibited by adrenaline (2 mug/ml); the inhibition was completely blocked by propranolol (0.5 mug/ml). 6 The results indicate the presence of an inhibitory beta-adrenoceptor and suggest the possibility of an excitatory alpha-adrenoceptor in guinea-pig urinary bladder.  (+info)

*  Beta-2 adrenergic antagonist
A Beta-2 adrenergic antagonist (β2-adrenoceptor antagonist) is an adrenergic antagonist which blocks the beta-2 adrenergic ... ICI-118,551 Butaxamine Propranolol Betablocker Beta-2 adrenergic receptor Beta2-adrenergic agonist Bilski, AJ; Halliday, SE; ... Fitzgerald, JD; Wale, JL (1983). "The pharmacology of a beta 2-selective adrenoceptor antagonist (ICI 118,551)". J Cardiovasc ... an antagonist for β2 and for β1 or β3 adrenoceptors) like the non-selective betablocker Propranolol. ...
*  Beta-3 adrenergic antagonist
A Beta-3 adrenergic antagonist (β3-adrenoceptor antagonist) is an adrenergic antagonist which blocks the Beta-3 adrenergic ... "Potent and selective human beta(3)-adrenergic receptor antagonists". The Journal of Pharmacology and Experimental Therapeutics ... SR 59230A Carvedilol Betablocker Beta-3 adrenergic receptor Candelore MR, Deng L, Tota L, Guan XM, Amend A, Liu Y, Newbold R, ... an antagonist for β3 and for β1 or β2 adrenoceptors) like the non-selective betablocker Carvedilol. ...
*  Brefonalol
... is a beta-adrenergic antagonist. Halabi, A; Endell, W; Halabi, I; Kirch, W (1990). "Hemodynamic effects of ...
*  Bucumolol
... is a beta-adrenergic antagonist. Nakayama, K; Oshima, T; Koike, H (1981). "Assessment of beta-blockade and the non- ... a beta-adrenergic blocking agent, on atrioventricular conduction in anesthetized dogs". Archives Internationales de ...
*  Levomoprolol
... is a beta adrenergic antagonist. It is the (S)-enantiomer of moprolol. Gianesello, V; Brenn, E; Figini, G; ... Gazzaniga, A (1989). "Determination by coupled high-performance liquid chromatography-gas chromatography of the beta-blocker ...
*  Diprafenone
... is an antiarrhythmic beta adrenergic antagonist. Koytchev, R; Alken, RG; Mayer, O; Smith, I; Greenwood, M (1996). " ...
*  Cetamolol
... is a beta adrenergic antagonist. Cardioselective b1-adrenergic blocker. Klausner, MA; Irwin, C; Mullane, JF; Shand, ...
*  History of hypertension
Black JW, Crowther AF, Shanks RG, Smith LH, Dornhorst AC (May 1964). "A new adrenergic beta receptor antagonist". Lancet. 1 ( ... The first member was verapamil, a derivative of papaverine that was initially thought to be a beta blocker and used for angina ... The British physician James W. Black developed beta blockers in the early 1960s; these were initially used for angina, but ... February 1996). "Nonpeptide angiotensin II receptor antagonists: the next generation in antihypertensive therapy". J. Med. Chem ...
*  Bornaprolol
... is a beta-adrenergic antagonist. Cheymol, G; Jaillon, P; Lecoq, B; Lecoq, V; Cheymol, A; Krumenacker, M (1987). " ... "Cardiovascular beta-adrenergic blocking effects of bornaprolol in humans: Relation to dose and plasma concentration". Journal ...
*  Bunitrolol
... is a beta-adrenergic antagonist. Haddad, S; Poulin, P; Funk, C (2010). "Extrapolating in vitro metabolic ...
*  History of catecholamine research
J. W. Black; A. F. Crowther; R. G. Shanks; A. C. Dornhorst (1964). "A new adrenergic beta-receptor antagonist". The Lancet. 283 ... as either alpha or beta adrenergic blocking drugs." Dichloroisoprenaline was the first beta blocker; it retains some intrinsic ... that both are beta type receptors. … It is suggested that this terminology be extended to the realm of adrenergic blocking ... he called beta adrenotropic receptor (now β-adrenoceptor or β-adrenergic receptor). ″This concept of two fundamental types of ...
*  Dorzolamide/timolol
Timolol is a non-selective beta-adrenergic antagonist. Common adverse effects include temporarily blurred vision, cloudy vision ...
*  Allium neapolitanum
... seems to have beta-adrenergic antagonist properties. The Plant List "BSBI List 2007". Botanical Society of ...
*  Radiocontrast agent
Adverse experience with cimetidine and safety of beta-adrenergic antagonists". Arch Intern Med. 145 (12): 2197-200. doi:10.1001 ... Previously, beta blockers have been assumed as risk factor for the acquisition of contrast medium-induced adverse reactions/ ... Due to recent investigations it became clear that beta blockers do not have the ability to increase the frequency of adverse ... Boehm I, Morelli J, Nairz K, Silva Hasembank Keller P, Heverhagen JT (2016). "Beta blockers and intravenous roentgen contrast ...
*  Moprolol
... is a beta-adrenergic antagonist, or beta blocker. Typically moprolol is prescribed to treat hypertension, high blood ... A similar beta-blocker, metoprolol, that is very popular both overseas and in the US brought in an estimated €2.2 million in ... One significant clinical study in hypertension ran in 2013 using non-selective beta-blocker to study the effects on lowering ... Wong, Gavin WK; Wright, James M. Blood pressure lowering efficacy of nonselective beta-blockers for primary hypertension. doi: ...
*  The Moscow International Medical Cluster
"Identification of adenylate cyclase-coupled beta-adrenergic receptors with radiolabeled beta-adrenergic antagonists". ...
*  Hobet Coal Mine
"Identification of adenylate cyclase-coupled beta-adrenergic receptors with radiolabeled beta-adrenergic antagonists". ...
*  IronFX
"Identification of adenylate cyclase-coupled beta-adrenergic receptors with radiolabeled beta-adrenergic antagonists". ...
*  Alpha blocker
Beta blocker Adrenergic antagonists Katzung, Bertram; Masters, Susan (2013). Basic and Clinical Pharmacology. Lange. ISBN 978-0 ... Non-selective α-adrenergic receptor antagonists include: Phenoxybenzamine Phentolamine Tolazoline Trazodon Selective α1- ... are a class of pharmacological agents that act as antagonists on α-adrenergic receptors (α-adrenoceptors). Historically, alpha- ... adrenergic receptor antagonists include: Alfuzosin Doxazosin Prazosin (inverse agonist) Tamsulosin Terazosin Silodosin ...
*  Pacrinolol
... is a beta adrenergic receptor antagonist. Stache, U; Fritsch, W; Fehlhaber, HW (1987). "Synthesis of the highly ... cardioselective beta-sympatholytic pacrinolol". Arzneimittel-Forschung. 37 (11): 1217-21. PMID 2894210. ...
*  Ersentilide
... is a beta adrenergic receptor antagonist. Lombardi, F; Terranova, P (2006). "Pharmacological treatment of atrial ...
*  Tienoxolol
... is a beta adrenergic receptor antagonist. Mahé, N; Do, B; Nicolaï, B; Rietveld, IB; Barrio, M; Tamarit, JL; Céolin, ...
*  Tiprenolol
... is a beta adrenergic receptor antagonist. Allen, JD; Shanks, RG (1974). "Effects of tiprenolol, practolol and ...
*  Spirendolol
... is a beta adrenergic receptor antagonist. Mostaghim, R; Maddox, YT; Ramwell, PW (1986). "Endothelial potentiation ... of relaxation response to beta adrenoceptor blocking agents". The Journal of Pharmacology and Experimental Therapeutics. 239 (3 ...
*  Pargolol
... is a beta adrenergic receptor antagonist. Hugues, FC; Julien, D; Bors, V; Mougeot, G; Marche, J (1980). "Determination ... in man of the beta blocking properties and the pharmacological half of pargolol (Author's transl)". Therapie. 35 (4): 475-81. ...
*  Bronchoconstriction
These medications include short-acting beta agonists (SABAs) such as albuterol which typically last 4-6 hours, and long-acting ... Muscarinic antagonists (anti-cholinergics): Blocking the muscarinic acetylcholine receptors in pulmonary smooth muscle tissue ... http://www.atsjournals.org/doi/abs/10.1164/rccm.201303-0437ST Rau, JL (Jul 2000). "Inhaled adrenergic bronchodilators: ... These medications include short-acting muscarinic antagonists (SAMAs) such as ipratropium, and long-acting muscarinic ...
Overall 25,517 (46.4%) patients in the study sample were prescribed beta-blockers at discharge. The rate of beta-blocker use declined as COPD or asthma severity increased (p , 0.001). Beta-blockers were prescribed for 50.3% of patients without COPD or asthma, 37.4% of patients with COPD or asthma not prescribed beta-agonists, 25.2% of patients with COPD or asthma prescribed beta-agonists, and 12.5% of patients with severe COPD or asthma. Over 91% of patients discharged on beta-blockers were prescribed beta1-selective agents. After adjusting for demographic and clinical factors, patients with COPD or asthma continued to be less likely to be prescribed beta-blocker therapy compared with patients without pulmonary disease (odds ratio [OR] 0.65) (95% confidence interval [CI] 0.62 to 0.69, for patients with COPD or asthma not prescribed beta-agonists, OR 0.38 [95% CI 0.34 to 0.41] for patients with COPD or asthma prescribed beta-agonists but not prescribed oral steroids or admitted in the prior year, ...
Postsystolic shortening (PSS), a positive myocardial velocity after aortic valve closure as assessed by tissue Doppler imaging (TDI), is a common finding in patients with myocardial disease. Beta-blocker therapy is shown to improve both global and regional myocardial function. The aim of the present study was to examine whether beta-blocker therapy might reduce incidence and magnitude of PSS in patients with nonischemic dilated cardiomyopathy. Before and a few months after beta-blocker (carvedilol) therapy, 19 patients (7 men and 12 women, age 59±13 years) underwent conventional echo-assessment and TDI. From the apical two, four, and long-axis views, we constructed time velocity curves at the 12 basal and mid-myocardial segments of the left ventricular (LV) walls. PSS was defined if the positive myocardial velocity after aortic valve closure was greater than the ejection peak (Figure⇓). The number of PSS was counted before and after beta-blocker therapy. Beta-blocker therapy decreased LV ...
Introduction: Catecolaminergic polymorphic ventricular tachycardia (CPVT) is an inherited cardiac disease which predisposes to exercise-induced life-threatening arrhythmias. The current therapeutic recommendations are beta-blocker therapy and ICD implantation. We aimed to determine the effect of beta-blocker treatment on exercise-induced arrhythmias in CPVT patients.. Methods: A total of 38 CPVT patients were followed for 24 (8-288) months. Of these, 8 were index patients and 30 were mutation positive family members diagnosed by cascade genetic screening. Clinical evaluation including exercise test was performed at inclusion and repeated 3 months after initiation of beta-blocker therapy in maximum tolerable doses. Heart rate and workload at occurrence of ventricular premature beats (VPB), couplets and non-sustained VT (nsVT) were recorded.. Results: Exercise-induced arrhythmias were observed in 28 (79 %) patients before treatment. Resting and maximum heart rate during exercise test were reduced ...
A recent study by Australian researchers suggests that cardiovascular medications known as beta-blockers can decrease the risk of osteoporosis-related bone fractures by half.
Cochrane, B., Quinn, S., Walters, H. and Young, I. (2012), Investigating the adverse respiratory effects of beta-blocker treatment: six years of prospective longitudinal data in a cohort with cardiac disease. Internal Medicine Journal, 42: 786-793. doi: 10.1111/j.1445-5994.2011.02563.x ...
The main finding of the present meta-analysis indicates that the effect of beta-blockers in patients with HF and AF is significantly different from the effect of these drugs in patients with HF and sinus rhythm. Indeed, beta-blockers were not found to have a favorable effect on HF hospitalizations or mortality in 1,677 AF patients who had been enrolled in placebo-controlled, randomized studies.. This finding is important as most patients with HF and AF receive beta-blocker treatment. Beta-blockade is recommended in the current guidelines for HF and AF treatment, albeit for different indications (1,23). In HF treatment guidelines, beta-blockers are recommended for all patients in order to reduce morbidity and mortality, without differentiation regarding rhythm. As such, these drugs are part of the standard medical therapy for all patients with HF and reduced LVEF. In addition, beta-blocker therapy has been shown to prevent new onset or recurrent AF in patients with HF (15,24) after myocardial ...
This analysis demonstrates that trial results of beta-blocker therapy in patients with CHF are consistent with a beneficial effect on total and cardiovascular mortality. The overall decrease in the odds of death was 31%, with one death prevented per 35 patients treated. The benefit from beta-blockade was consistent over the studies examined; however, it was most pronounced in the studies of carvedilol, which account for 55% of all included patients.. Previous studies, including a meta-analysis ([21]), have demonstrated that beta-blockade can improve left ventricular ejection fraction, symptoms and morbidity indices ([14-20]). The finding of improved mortality with beta-blockade has also been suggested by many previous studies, but most have lacked the statistical power to find even moderate improvements in survival ([14, 15, 17, 18, 33, 38, 42-44, 49, 56]). The results from this meta-analysis increase confidence in the hypothesis that beta-blockade reduces mortality in heart failure.. Previous ...
A common practice used to control autonomic responses during surgery is to administer beta-blockers intraoperatively. This practice has been shown to effectively blunt autonomic responses to intraoperative events. Several studies have shown that administration of beta-blockers can decrease intraoperative anesthetic requirements. Additionally, it has been demonstrated in several studies that intraoperative beta-blocker administration may actually decrease postoperative pain scores and opioid requirements, although these results are not entirely consistent. The mechanism by which the decrease in postoperative pain and narcotic requirements occurs is unclear. It has been postulated that esmolol may itself possess some analgesic-like properties, as was suggested by studies performed in rodent models. It has also been postulated that perioperative beta-blockade may attenuate the neuroendocrine stress response to surgery, thereby decreasing inflammatory responses in tissues; however, this theory was ...
According to the reports from Ministry of Health in each country, the average life spans were expanded over the past century. This trend is expected to be extended furt..
Andrews et al performed the first meta-analysis in this area. They found that 13 of 19 studies investigating the benefit of prophylactic beta-blockers showed a significant benefit in favour of giving prophylaxis. Pooling all these results showed a reduction in AF from 34% to 8.7% from studies involving 1,549 patients. Interestingly no difference was shown when pre-operative beta-blocker studies were compared to post-operative studies. No benefit was shown in 8 studies assessing either verapamil or digoxin as AF prophylaxis. They also showed that the mean ventricular rate was significantly lower in beta-blocked patients when they did go into AF, with a mean rate 24bpm slower than controls. They did caution that most patients in these studies were young, male and had good ejection fractions and had been on beta-blockers pre-operatively. Kowey et al in 1992 pooled data from 7 studies containing 1,418 patients, and found a reduction in AF from 20% to 9.8%. In addition they pooled data from 2 studies ...
Aims: We sought to: (1) estimate the proportion of patients who initiated beta-blocker therapy after acute myocardial infarction (AMI) in Regione Emilia-Romagna (RER); (2) examine predictors of post-AMI beta-blocker initiation; and (3) assess adherence to such therapy. Methods and Results: Using healthcare claims data covering all of RER, we identified a cohort of 24,367 patients with a hospitalization for AMI between 2004 and 2007, who were discharged from the hospital alive and without contraindications to beta-blocker therapy. We estimated the proportion of eligible patients with at least one prescription for a beta-blocker following discharge and performed a multivariable logistic regression analysis to identify independent predictors of post-AMI beta-blocker initiation. We computed the proportion of days covered (PCD) as a measure of medication adherence at 6 and 12 months post-discharge. Following discharge, 16,383 (67%) cohort members initiated beta-blocker therapy. Independent predictors of beta
Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Ivabradine acts by selectively inhibiting the
Beta-blockers, a type of drug frequently prescribed for people with heart disease, may not reduce the risk of a second heart attack, death, or stroke in people with coronary artery disease (CAD). In people with risk factors for heart disease, beta-blockers may increase the risk of such events, according to findings from a recent large observational study conducted by a team of investigators from the Cardiac and Vascular Institute at NYU Langone Medical Center.
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A total of 18,254 participants were assessed, of which 13,946 (76.4%) were in sinus rhythm and 3,066 (16.8%) in AF. Crude death rates over a mean follow-up of 1.5 years (SD 1.1) were 16.0% in sinus rhythm and 20.7% in AF. Beta-blocker therapy in patients with sinus rhythm led to a significant reduction in all-cause mortality (HR 0.73, 0.67-0.80; p,0.001) and CV-hospitalisation (HR 0.78, 0.73-0.83; p,0.001), as well as CV-death, HF-hospitalisation, the composite of all-cause mortality/CV-hospitalisation and the composite of CV-death/HF-hospitalisation. In contrast, there was no apparent effect from beta-blockers on any outcome in patients with AF, including mortality (HR 0.97, 0.83-1.14; p=0.73) and CV-hospitalisation (HR 0.91, 0.79-1.04; p=0.15). All outcomes demonstrated significant interaction p-values for beta-blocker efficacy according to baseline rhythm. The lack of efficacy for mortality was seen across all AF sub-groups. AF patients had more frequent CV-hospitalisation and longer length ...
Learn more about Preventive Cardiology: Beta-blockers at Kendall Regional Medical Center Current UsesHow Beta-Blockers WorkWhat You Should Knowrevision ...
Between June 2004 and April 2008, 497 statin-naive patients scheduled for vascular surgery were included in the trial at Erasmus MC Rotterdam, The Netherlands. Patients were randomised to receive either placebo or fluvastatin extended release at a dose of 80mg once daily. Treatment was started at the outpatient clinic on the day of randomisation, median 37 days prior to the surgical procedure and was continued at least during the first 30 days after surgery. Inflammatory markers at baseline, including hs-CRP and IL-6 were assessed in patients allocated to fluvastatin or placebo. At hospital, admission levels of hs-CRP and IL-6 were significantly lower in patients on fluvastatin (respectively 6mg/L vs. 4.66mg/L, p=.030 and 8.45pg/mL vs 5.75pg/mL, p=.024). The primary analysis was intention-to-treat and involved all patients who were randomly assigned to either fluvastatin or placebo. Directly after surgery, study treatment was temporarily discontinued in 115 (23%) patients for a median duration ...
Abstract The caffeine-induced impairment of insulin action is commonly attributed to adenosine receptor (AR) antagonism in skeletal muscle. However, epinephrine, a potent inhibitor..
Methods and Results-The study included 5926 consecutive patients who underwent CABG and were discharged alive. The prevalence and consistency of β-blocker use were determined in patients with and without a history of myocardial infarction (MI). β-Blockers were always used in 1280 patients (50.9%) with and 1642 patients (48.1%) without previous MI after CABG. Compared with always users (n=2922, 49.3%), the risk of all-cause death was significantly higher among inconsistent β-blocker users (hazard ratio [HR], 1.96; 95% confidence interval [CI], 1.50-2.57), and never using β-blockers was associated with increased risk of both all-cause death (HR, 1.42; 95% CI, 1.01-2.00) and the composite of adverse cardiovascular events (HR, 1.29; 95% CI, 1.10-1.50). In the cohort without MI, the HR for all-cause death was 1.70 (95% CI, 1.17-2.48) in inconsistent users and 1.23 (95% CI, 0.76-1.99) in never users. In the MI cohort, mortality was higher for inconsistent users (HR, 2.14; 95% CI, 1.43-3.20) and ...
The Aim is to define the contribution of genetic variation to the interindividual variability in response to β-blockade. The rationale for the study is as follows: Beta-blockers prevent the activation of β-ARs and thus form the cornerstone of treatment of pathological states such as congestive heart failure and coronary artery disease. Functional polymorphisms in cardiac beta-receptors have been shown to determine response to β-blocker therapy. A physiologic stimulus such as exercise causes sympathetic stimulation and activation of the cardiac β-ARs and genotypic differences in response to β-blockers are magnified under states of heightened sympathetic activity. Thus, in addition to measuring the response to β-blockers at rest, we will also determine the response to β-blockade after sub-maximal exercise on a supine bicycle ergometer. Genetic variations that may alter sensitivity to a beta blocker will be sought ...
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Beta blockers generally arent used in people with asthma because of concerns that the medication may trigger severe asthma attacks. In people who have diabetes, beta blockers may block signs of low blood sugar, such as rapid heartbeat. Its important to monitor your blood sugar regularly.. Beta blockers can also affect your cholesterol and triglyceride levels, causing a slight increase in triglycerides and a modest decrease in high-density lipoprotein, the "good" cholesterol. These changes often are temporary. You shouldnt abruptly stop taking a beta blocker because doing so could increase your risk of a heart attack or other heart problems.. ...
Assumption: Precaution is needed when taking any medication during pregnancy. Beta-blockers for high blood pressure are included. TRUE Although beta-blockers taken during pregnancy can help lower blood pressure, babies whose mothers took beta-blockers grew more slowly than average babies. http://www2.cochrane.org/reviews/en/ab002863.html My Views: Of course, your care provider must help you weigh the benefits and risks…
First, before I forget, extreme nausea can be a symptom that heart failure is worsening. Personally, though, Id expect it to become progressively worse, not to come rampaging out of nowhere the way it did - I still suspect Nebivolol was the culprit. I will, however, bear it in mind and keep a close eye…
A new study adds to doubts about using beta blockers to reduce the risks of surgery. The death rate for people given beta blockers before non-cardiac surgery wa
Nebivolol, (bystolic, nebilet, nebil) is a long acting cardioselective beta-blocker at present approved for the therapy of high blood pressure. Nebivolol is
beta blocker: A blocking agent, one of a class of drugs used to treat hypertension and control the rate at which the heart beats.
Beta-blockers (also known as beta-adrenoceptor blocking agents) are medications used to treat several conditions, often by decreasing heart activity.
1 Answer - Posted in: heart attack, weight, beta blocker, prescription - Answer: Hi You have a difficult situation. However, the best way to lose ...
The heart is a muscle that contracts in rhythmic sequence for the duration of our lifetime. Each beat is stimulated by an electrical signal that is ge...
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Objectives The purpose of this study was to compare the efficacy of beta-blockers in congenital long QT syndrome (LQTS). Background Beta-blockers are the mainstay in managing LQTS. Studies comparing the efficacy of commonly used beta-blockers are lacking, and clinicians generally assume they are equally effective.. Methods Electrocardiographic and clinical parameters of 382 LQT1/LQT2 patients initiated on propranolol (n = 134), metoprolol (n = 147), and nadolol (n = 101) were analyzed, excluding patients ,1 year of age at beta-blocker initiation. Symptoms before therapy and the first breakthrough cardiac events (BCEs) were documented.. Results Patients (56% female, 27% symptomatic, heart rate 76 +/- 16 beats/min, QTc 472 +/- 46 ms) were started on beta-blocker therapy at a median age of 14 years (interquartile range: 8 to 32 years). The QTc shortening with propranolol was significantly greater than with other beta-blockers in the total cohort and in the subset with QTc ,480 ms. None of the ...
Looking for online definition of Adrenergic beta-antagonists in the Medical Dictionary? Adrenergic beta-antagonists explanation free. What is Adrenergic beta-antagonists? Meaning of Adrenergic beta-antagonists medical term. What does Adrenergic beta-antagonists mean?
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Purified sarcolemmal and light vesicle (intracellular) fractions of beta-adrenergic receptors were used to examine the effects of propranolol on receptor translocation in guinea pig heart. Guinea pigs were given propranolol (0.15 mg/kg/hr) via minipumps for 7 days and either killed or made ischemic for 1 hour via a coronary ligature. Propranolol treatment led to an externalization of beta-receptors from light vesicle to sarcolemmal fractions. This externalization increased the number of surface beta-adrenergic receptors that were functional, as assessed by isoproterenol-stimulated adenylate cyclase activity. After chronic propranolol treatment, ischemia did not further alter receptor distribution. These results suggest that externalization of beta-adrenergic receptors from a light vesicle fraction to the sarcolemma contributes to up-regulation of beta-receptors that occur in response to both propranolol treatment and ischemia. Because propranolol-treated animals show blunting in externalization ...
Adrenergic beta-blocking agents were given to 7 patients with advanced congestive cardiomyopathy who had tachycardia at rest (98 plus or minus 13 beats/min). The patients were on beta-adrenergic receptor blockade for 2 to 12 months (average 5-4 months). One patient was given alprenolol 50 mg twice daily and the other patients were given practolol 50 to 400 mg twice daily. Virus infection had occurred in 6 of the patients before the onset of symptoms of cardiac disease. All patients were in a steady state or were progressively deteriorating at the start of beta-adrenergic receptor blockade. Conventional treatment with digitalis and diuretics was unaltered or reduced during treatment with beta-blocking agents. An improvement was seen in their clinical condition shortly after administration of the drugs. Continued treatment resulted in an increase in physical working capacity and a reduction of heart size. Noninvasive investigations including phonocardiogram, carotid pulse curve, apex cardiogram, ...
Exercise training and beta-blocker treatment ameliorate age-dependent impairment of beta-adrenergic receptor signaling and enhance cardiac responsiveness to adrenergic stimulation. Am J Physiol Heart Circ Physiol 293: H1596-H1603, 2007. First published June 8, 2007; doi:10.1152/ajpheart.00308.2007.- Cardiac beta-adrenergic receptor (*-AR) signaling and left ventricular (LV) responses to beta-AR stimulation are impaired with aging. It is shown that exercise and beta-AR blockade have a favorable effect on cardiac and vascular *-AR signaling in several cardiovascular diseases. In the present study, we examined the effects of these two different strategies on *-AR dysregulation and LV inotropic reserve in the aging heart. Forty male Wistar-Kyoto aged rats were randomized to sedentary, exercise (12 wk treadmill training), metoprolol (250 mg kg-1 day-1 for 4 wk), and exercise plus metoprolol treatment protocols. Ten male Wistar- Kyoto sedentary young rats were also used as a control group. Old ...
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A non-selective beta-adrenergic antagonist … A non-selective beta-adrenergic antagonist with a long half-life, used in cardiovascular disease to treat arrhythmias, angina pectoris, and hypertension. Nadolol is also used for migraine disorders and for tremor. (PubChem) Pharmacology: Nadolol is a nonselective beta-adrenergic receptor antagonist with a long half-life, and is structurally similar to propranolol. Clinical pharmacology studies have demonstrated beta-blocking activity by showing (1) reduction in heart rate and cardiac output at rest and on exercise, (2) reduction of systolic and diastolic blood pressure at rest and on exercise, (3) inhibition of isoproterenol-induced tachycardia, and (4) reduction of reflex orthostatic tachycardia. Nadolol has no intrinsic sympathomimetic activity and, unlike some other beta-adrenergic blocking agents, nadolol has little direct myocardial depressant activity and does not have an anesthetic-like membrane-stabilizing action. Mechanism of action: Like ...
One other option is the use of metoprolol succinate, which is known as a beta blocker. These are very common when used to treat both hypertension and cardiac ischemia. They work by limiting the bodys ability to produce epinephrine, which is basically just adrenaline. Many people are familiar with the way that adrenaline works from sports or stressful situations, in which it can flood the body with energy. This also causes the persons heart to beat quickly or to beat harder, both of which can increase blood pressure. To a smaller degree, epinephrine is always doing this, even when there is no notable increase due to outside stimuli.. The beta blockers lower the production levels without stopping them completely, and so less epinephrine means that the heart does not work as aggressively. It slows down, pumping less blood and working less vigorously to do so. This takes a lot of pressure off of the artery walls, therefore reducing the risk of issues like cardiac ischemia, stroke, and the like. ...
Effects of some beta-adrenergic blockers on male fertility parameters in rats.: The effects of atenolol (9 and 18 mg/kg.b.wt.), metoprolol (3.5 and 7 mg/kg.b.wt
Objective To determine the effect of perioperative blocker treatment in patients having non-cardiac surgery. confidence interval 0.16 to 1 1.24) for the composite outcome of cardiovascular mortality, non-fatal myocardial infarction, and non-fatal cardiac arrest. Methods adapted from formal interim monitoring boundaries applied to cumulative meta-analysis showed that the evidence failed, by a considerable degree, to meet standards for forgoing additional studies. Picroside I The individual safety outcomes in patients treated with perioperative blockers showed a member of family risk for bradycardia requiring treatment of 2.27 (95% CI 1.53 to 3.36, 99% CI 1.36 to 3.80) and a nominally statistically significant family member risk for hypotension needing treatment of just one 1.27 (95% CI 1.04 to at least one 1.56, 99% CI 0.97 to at least one 1.66). Summary The data that perioperative blockers decrease major cardiovascular occasions is motivating but as well unreliable to permit definitive ...
We studied 820 people who take Metoprolol succinate and Tramadol from FDA. Drug interactions are found. See what they are, when they happen and for whom.
This study was carried out to examine the effects of acute and chronic stress on hematological parameters in combination with β-adrenergic receptor blockade in rats. In the present study, acute stress is a form of short-term stress induced by a single footshock session, and chronic stress is a form of long-term stress induced by multiple and repetitive footshock sessions. Male Wistar rats were treated with propranolol (5 mg/kg s.c.) and were subjected to an acute stress [intermittent session of footshock: 0.5 mA, during 60s (5s shock, 5s pause) at one and three days after the moment of propranolol administration] and to a chronic stress [intermittent session of footshock: 0.5 mA, during 60s (5s shock, 5s pause) over three consecutive days from the moment of propranolol administration]. Control group rats were subjected to the same conditions without the propranolol administration and were treated with saline solution. Four days after the drug administration, we assessed the number of total ...
Adrenergic beta-blockade is the most potent pharmacological therapy for the improvement of global left ventricular (LV) function in heart failure. A substantial portion of patients responds poorly to beta-blockers, but there is scarce information about LV regional function and recovery. We intended to evaluate the effects of beta-blockade on LV regional function and recovery, contractile reserve (CR) and response to long-term treatment.MethodsTwenty-two patients with heart failure were investigated at rest and during dobutamine stress echocardiography (DSE), before and after 6 months of metoprolol treatment. LV function was evaluated by global ejection fraction (EF), and by regional function in basal, mid and apical segments.ResultsRecovery of LV global function (increase in EF |5%) after metoprolol treatment was significantly and best correlated to CR in basal segments of the ventricle (r=0.79, pr=0.55, p=0.007. In a multivariate logistic regression, including global and regional CR, age, gender,
4 days, P 0. e. In children with very high hyperopia (greater than 8 diopters), the accom- modative demand may be so high that the child simply вgives blo ckers, developing bilateral profound beta blockers propranolol migraine amblyopia with straight eyes. 2 Effect of Mobile Phase pH Mobile phase pH can have significant impact on the chromatographic background as well.
Propranolol treatment - Hi This kind of thing is new to me so please bare with me (thanks) Am looking for any mums on here who are currently......
Before you begin using a medication, be sure to inform your doctor of any medical conditions or allergies you may have, any medications you are taking, whether you are pregnant or breast-feeding, and any other significant facts about your health. These factors may affect how you should use this medication.. Asthma and other breathing problems: Acebutolol and other beta-blockers may cause symptoms of asthma to worsen. Low doses of acebutolol may be used with caution by people with asthma who do not respond to or who cannot tolerate other treatment.. Heart failure: This medication may make the symptoms of congestive heart failure worse, by slowing down the heart rate and heartbeat strength. If you have congestive heart failure, discuss with your doctor how this medication may affect your medical condition, how your medical condition may affect the dosing and effectiveness of this medication, and whether any special monitoring is needed.. Kidney function: Kidney disease or reduced kidney function ...
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Long QT syndrome is the most commonly recognised cause of sudden cardiac death in children. With a prevalence of 1 in 2000, family screening is identifying large numbers of hitherto asymptomatic gene carriers in the community, about a third of whom have a normal QT interval. The mainstay of treatment is long term uninterrupted beta blocker therapy, a treatment with many potential side effects. This article reviews the evidence and suggests a cohort who may, after assessment in a specialised cardiac-genetic clinic, be spared this treatment because of very low baseline risk. These are asymptomatic boys and prepubertal girls with a heart rate corrected QT interval persistently less than 470 ms who do not indulge in high risk activities (especially swimming) and do not have a missense mutation in the c-loop region of the KCNQ1 (long QT 1) gene.. ...
5. The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension and of the European Society of Cardiology. (PDF) 2007 Guidelines for the management of arterial hypertension. Eur Heart J 2007; 28: 1462-1536. 6. Agabiti Rosei E, Rizzoni D. Metabolic profile of nebivolol, a beta-adrenoceptor antagonist with unique characteristics. Drugs 2007; 67: 1091-1107. 7. Giugliano D, Acampora R, Marfella R, de Rosa N, Ziccardi P, Ragone R, de Angelis L, dOnofrio F. Metabolic and cardiovascular effects of carvedilol and atenolol in non-insulin-dependent diabetes mellitus and hypertension - a randomized, controlled trial. Ann Intern Med 1997; 126: 955-959. 8. Brixius K, Bundkirchen, Bolck B et al. Nebivolol, bucindolol, metoprolol and carvedilol are devoid of intrinsic sympathomimetic activity in human myocardium. Br J Pharmacol 2001; 133: 1330-1338. 9. Maack C, Tyroller S, Schnabel P, Cremers B, Dabew E, Südkamp M, Böhm M. Characterization of beta-selectivity, ...
Alpha- and beta-blocking drugs are used in the treatment of hypertension, and when 1 drug can combine the receptor blockade, it should be expected to enhance therapeutic outcomes. Carvedilol, a nonselective beta-blocker with selective alpha-1 blocking actions, appears to offer better results than agents possessing only 1 variety of receptor-blocking activity. Carvedilol is available in 3.125-, 6.25-, 12.5-, and 25- mg tablet strengths from Apotex Inc, Caraco Pharmaceutical Laboratories, and Mylan Laboratories. The beneficial actions for beta-blockers in congestive heart failure are based on theoretical action, suggesting a decrease of sympathetic outflow at the cardiac level or an alteration in renin release. The additional effect of alpha-1 blockade with carvedilol results in general peripheral arterial and venous dilation, with the effects on standing blood pressure being the most pronounced. In general, beta-blockers are indicated for the treatment of hypertension, angina, and heart failure. ...
Objectives Combination therapy with methotrexate (MTX) and tumour necrosis factor (TNF) blockade has increased remission rates in patients with rheumatoid arthritis. However, there are no guidelines regarding cessation of therapy. There is a need for markers predictive of sustained remission following cessation of TNF blocker therapy.. Methods Patients in remission (DAS28 ,2.6) treated with a TNF blocker and MTX as initial or delayed therapy were recruited. Joints were assessed for grey scale synovitis and power Doppler (PD) activity. Immunological assessment involved advanced six-colour flow cytometry.. Results Of the 47 patients recruited, 27 had received initial treatment and 20 delayed treatment with TNF blocking drugs. Two years after stopping TNF blocker therapy, the main predictor of successful cessation was timing of treatment; 59% of patients in the initial treatment group sustained remission compared with 15% in the delayed treatment group (p=0.003). Within the initial treatment group, ...
This trial investigated the efficacy and tolerability of carvedilol in Japanese patients with mild-to-moderate chronic heart failure. The primary endpoint was a
The following is my true testimony only and I do not advise ANYONE to do what I did but please first consult your doctor. For years I have suffered from arrhythmia and was on put on beta-blockers for years by my doctor but it was as good as not taking them at all because the rapid heartbeat came anyway and suddenly with shortness of breath and dizziness. I thought what was the use of these medications I might as well try a natural supplement that might help. I am one of those daring ones so I first prayed and asked God to show me what would be best for my heart. I stopped the beta-blockers on my own. Long story short, within days I found Natures Answer Hawthorne Tincture. I didnt take it right away but kept it handy to take when my heart went rapid and then one day I climbed a few steps at the subway, I went out of breath and the problem began real bad this time and I was alone. I opened the bottle and squeezed a few droppers in my mouth and took a gulp of water which too, I never fail to ...
Our study has several important limitations. First, selection bias regarding the use of β-blockers is unavoidable in observational studies. Although we used a propensity score to adjust for baseline β-blocker use, we could not exclude the influence of unmeasured confounders on clinical outcomes. However, as listed in our tables (tables 1-3), all of our demographic and operative characteristics had postmatching standard reference values less than 0.1; standardized differences of 0.2, 0.5, and 0.8 represent small, medium, and large effect sizes, respectively.32 Second, we did not have clarification of MI history (recent vs. nonrecent or description of time since MI). This might have been useful in identifying the role of β-blockers, particularly because the benefit of β-blockers observed in early studies may been driven by those with recent MIs, a cohort known to benefit from aggressive β-blockade. Third, our analyses of β-blocker use were limited to class effects and categorical/qualitative ...
Learn more about Preventive Cardiology: Beta-blockers at Frankfort Regional Medical Center Current UsesHow Beta-Blockers WorkWhat You Should Knowrevision ...
Food to avoid with metoprolol - Why do I need to take metoprolol tartrate with food? Absorption increased. Food increases absorption. Metoprolol serum levels may be increased if taken with food. For this reason it is advised to take immediate release tartrate tablets with food; metoprolol succinate can be taken with or without food.
Hello, and thanks for much for reading this!! My 21-year old son was diagnosed with Marfan Syndrome at age 6. He has been on beta-blockers since that time. During his childhood and teen years, he ha...
IV cardiac medication reference pocket card for pressors, beta blockers, calcium channel blockers, and vasodilators. Reference heart rate, systemic vascular resistance, cardiac output, central venous pressure with receptor activation chart. Cardiac Medica
Learn more about Beta-blockers at Medical City Dallas Coenzyme Q 10 (CoQ 10 ) -Supplementation...
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Beta-Blocker Therapy in Noncardiac Surgery. Poldermans, Don; Boersma, Eric // New England Journal of Medicine;7/28/2005, Vol. 353 Issue 4, p412 Comments on the use of beta-blockers in noncardiac surgery. Risk for death from myocardial infarction among patients receiving noncardiac surgery in the U.S.; Use of beta-blockers to regulate oxygen use in the heart following surgery; Need for clinical trials on the benefits of beta-blockers;... ...
The authors of this large meta-analysis identified 60 studies that met their inclusion criteria (randomized controlled trials examining beta-blocker use in patients with AMI); they divided studies into pre-reperfusion-era ("early," before stents, thrombolytics, etc) and reperfusion-era ("modern era"). They found that, while in the early studies, beta-blockers conferred significant survival benefit (incident rate ratio [IRR] 0.86; 95% confidence interval [CI], 0.79-0.94), in the modern era they did not (IRR 0.98; 95% CI, 0.92-1.05). In the modern era, beta-blockers did reduce angina and reinfarction rates, but only in the first 30 days, and they increased the rates of heart failure and cardiogenic shock. The authors hypothesized that reperfusion technologies are so effective nowadays that any added benefit from beta-blockers is minimal. ...
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Beta Blockers can be effective in treating Congestive Heart Failure (CHF). Learn about Beta Blockers, see related evidence, and find other smart treatments for Congestive Heart Failure (CHF) at FoundHealth.
This discussion, from the Medscape website, gives an insight into the response that occurred at the AHA meeting in Orlando when the POISE study results where first presented (watch for the full paper in a journal soon). Chief investigator, PJ Devereaux says "I would certainly not recommend it to my mother". Experts in the discussion where divided whether beta blocker should be initiated for at risk patients presenting for high risk surgery. ...
The reason for the change is that the benefits have been found to far exceed the risks, says the American Diabetes Association (ADA). Beta-blockers are...
The odds reductions due to angiotensin-converting enzyme/angiotensin receptor blocker treatment estimated from the meta-analysis were as follows: CV death: 13%, P b .0001; nonfatal myocardial infarction: 16%, P = .00001; nonfatal stroke: 14%, P = .006; heart failure: 28%, P b .00001; hospitalization for angina: 7%, P = .02; and revascularization: 5%, P = .17. For the CV composites, the projected odds reduction was larger (17.8%, 95% CI 0.452-1.189) for the narrower composite compared with the extended CV composite (11.7%, 95% CI 0.623-1.136); that is, use of the extended composite reduced power to detect a difference between treatment groups ...
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In May, Dr. Reddys Laboratories issued a voluntary recall for 13,560 bottles of its hypertension drug metoprolol succinate extended release. According to the U.S. Food and Drug Administration (FDA), the drugs inability to pass a dissolution test prompted the United States recall, which became effective on May 23, 2014.
The last article I wrote about beta blockers was written last Summer when I was more or less just starting the beta blocker. I had noticed a decrease in performance and exercise tolerance and when I went to the cardiologist and had an echocardiogram it was determined that my rate was going up and my…
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Buy Propranolol online (Propranolol) discount for sale price best cheap order , Propranolol is a beta-blocker. Beta-blockers affect the heart and circulation (blood flow through arteries and veins).
Dr. Person responded: Yes. Beta blockers are strongly indicated in a post CABG patient. The vast majority of patients with a left |a href="/topics/bundle-branch-block" track_data="{
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Originally developed for heart problems, beta blockers are now commonly prescribed for anxiety. But what are the benefits and side effects?
Originally developed for heart problems, beta blockers are now commonly prescribed for anxiety. But what are the benefits and side effects?
The use of beta-blockers in older adults with stable angina who underwent PCI did not reduce the adjusted mortality rate, MI, stroke or revascularization, according to retrospective, observational registry analysis.
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August 31, 2012 Health Care, Medicine Comments Off Perioperative beta-blockade reduces postoperative adverse cardiac events in both the short and long term, and current guidelines recommend prophylactic beta-blockade for high-risk patients undergoing noncardiac surgery.. In this retrospective study, 30-day mortality (1% in the atenolol group vs 3% in the metoprolol group; P , .001) and 1-year mortality (7% vs 13%, respectively; p , .001) differed between the 2 beta-blockers.. The investigators concluded that perioperative beta-blockade using atenolol is associated with reductions in both short- and long-term postoperative mortality compared with metoprolol.. In 2009, on the basis of evidence from many studies, the American College of Cardiology/American Heart Association updated their guidelines, stating that perioperative beta-blockade is a class IIa recommendation for patients with cardiac risk and should be considered during surgery.. ...
TY - JOUR. T1 - Bucindolol displays intrinsic sympathomimetic activity in human myocardium. AU - Andréka, P.. AU - Aiyar, Nambi. AU - Olson, Leslie C.. AU - Wei, Jian Qin. AU - Turner, Mark S.. AU - Webster, Keith A.. AU - Ohlstein, Eliot H.. AU - Bishopric, Nanette H.. PY - 2002/5/21. Y1 - 2002/5/21. N2 - Background - Most clinical studies have shown that β-adrenergic receptor antagonists improve long-term survival in heart failure patients. Bucindolol, a nonselective β-receptor blocker, however, failed to reduce heart failure mortality in a recent large clinical trial. The reasons for this failure are not known. Bucindolol has partial agonist properties in rat myocardium, but whether it has agonist activity in human heart is controversial. To address this, we measured the ability of bucindolol to increase cAMP accumulation in human myocardium. Methods and Results - Myocardial strips (≈ 1 mm3) obtained from rat and nonfailing human hearts were confirmed to be viable for ≥48 hours in ...
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Penbutolol is a β-1,β-2 (nonselective) adrenergic receptor antagonist. Experimental studies showed a dose-dependent increase in heart rate in reserpinized (norepinephrine-depleted) rats given penbutolol intravenously at doses of 0.25 to 1.0 mg/kg, suggesting that penbutolol has some intrinsic sympathomimetic activity. In human studies, however, heart rate decreases have been similar to those seen with propranolol.. Penbutolol antagonizes the heart rate effects of exercise and infused isoproterenol. The β-blocking potency of penbutolol is approximately 4 times that of propranolol. An oral dose of less than 10 mg will reduce exercise-induced tachycardia to one-half its usual level; maximum antagonism follows doses of 10 to 20 mg. The peak effect is between 1.5 and 3 hours after oral administration. The duration of effect exceeds 20 hours during a once-daily dosing regimen. During chronic administration of penbutolol, the duration of antihypertensive effects permits a once-daily dosage ...
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ACT Latanoprost/Timolol: This is a combination product containing two different medications: latanoprost and timolol. Latanoprost belongs to a class of medications called prostaglandin analogs. It works to reduce the pressure in the eye by allowing fluid in the eye to flow better. Timolol belongs to a class of medications called beta-adrenergic receptor blockers (also known as beta-blockers). Latanoprost - timolol solution is available in an eye-drop form. It is used to reduce the pressure inside the eye for people with open-angle glaucoma or intraocular hypertension (increased pressure in the eye).
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Adrenergic beta Antagonists. Drugs that bind to but do not activate beta-Adrenergic Receptors thereby blocking the actions of ... beta-Adrenergic Agonists. Adrenergic beta-antagonists are used for treatment of Hypertension, Cardiac Arrhythmias, Angina ...
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Comparison of Adrenergic Beta-receptor Antagonists in Angina Pectoris | The BMJ  Comparison of Adrenergic Beta-receptor Antagonists in Angina Pectoris | The BMJ
Comparison of Adrenergic Beta-receptor Antagonists in Angina Pectoris Br Med J 1973; 1 :138 ... Comparison of Adrenergic Beta-receptor Antagonists in Angina Pectoris. Br Med J 1973; 1 doi: https://doi.org/10.1136/bmj.1.5846 ... suggests that metabolic breakdown products are probably of therapeutic importance only in so far as they antagonize beta- ...
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Nadolol is a nonselective beta-adrenergic receptor antagonist with a long half-life, and is structurally similar to propranolol ... Nadolol has no intrinsic sympathomimetic activity and, unlike some other beta-adrenergic blocking agents, nadolol has little ... Although cardiac failure rarely occurs in properly selected patients, patients being treated with beta-adrenergic blocking ... Clinical pharmacology studies have demonstrated beta-blocking activity by showing (1) reduction in heart rate and cardiac ...
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Binding of adrenergic beta-receptor antagonists to human serum albumin. - Semantic Scholar  Binding of adrenergic beta-receptor antagonists to human serum albumin. - Semantic Scholar
Binding of adrenergic beta-receptor antagonists to human serum albumin. by C Appelgren et al. ... Binding of adrenergic beta-receptor antagonists to human serum albumin.. @article{Appelgren1974BindingOA, title={Binding of ... adrenergic beta-receptor antagonists to human serum albumin.}, author={C Appelgren and Karl O. Borg and Rolf Elofsson and Karl ... The relationship between beta-adrenoceptors and adrenergic responsiveness in trout (Oncorhynchus mykiss) and eel (Anguilla ...
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A Beta-2 adrenergic antagonist (β2-adrenoceptor antagonist) is an adrenergic antagonist which blocks the beta-2 adrenergic ... ICI-118,551 Butaxamine Propranolol Betablocker Beta-2 adrenergic receptor Beta2-adrenergic agonist Bilski, AJ; Halliday, SE; ... Fitzgerald, JD; Wale, JL (1983). "The pharmacology of a beta 2-selective adrenoceptor antagonist (ICI 118,551)". J Cardiovasc ... an antagonist for β2 and for β1 or β3 adrenoceptors) like the non-selective betablocker Propranolol. ...
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A Beta-3 adrenergic antagonist (β3-adrenoceptor antagonist) is an adrenergic antagonist which blocks the Beta-3 adrenergic ... "Potent and selective human beta(3)-adrenergic receptor antagonists". The Journal of Pharmacology and Experimental Therapeutics ... SR 59230A Carvedilol Betablocker Beta-3 adrenergic receptor Candelore MR, Deng L, Tota L, Guan XM, Amend A, Liu Y, Newbold R, ... an antagonist for β3 and for β1 or β2 adrenoceptors) like the non-selective betablocker Carvedilol. ...
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Screening for potential beta 2-adrenergic receptor antagonists using CypHer5E and IN Cell Analyzer 1000 ( 		               ...  Screening for potential beta 2-adrenergic receptor antagonists using CypHer5E and IN Cell Analyzer 1000 ( ...
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Histamine H2 Antagonists. *Alpha/Beta Adrenergic Agonists. *Local Anesthetics, Amides. *Show All ... Alpha/Beta Adrenergic Agonists. Class Summary. These agents may be used to treat nasal congestion. ... Histamine H2 Antagonists. Class Summary. H2 blockers are reversible competitive blockers of histamine at H2 receptors, ... Histamine 2 (H2)-receptor antagonists should be administered preoperatively to prevent increase in gastric secretion during the ...
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AID 1135146 - Antagonist activity at guinea pig atrial beta adrenergic receptor assessed as isometric contractions at 5 x 10-5...  AID 1135146 - Antagonist activity at guinea pig atrial beta adrenergic receptor assessed as isometric contractions at 5 x 10'-5...
Antagonist activity at guinea pig atrial beta adrenergic receptor assessed as isometric contractions at 5 x 10-5 M by force ...
more infohttps://pubchem.ncbi.nlm.nih.gov/bioassay/1135146
Impact of beta blockade therapy on long-term mortality after ST-segment elevation acute myocardial infarction in the...  Impact of beta blockade therapy on long-term mortality after ST-segment elevation acute myocardial infarction in the...
Adrenergic beta-Antagonists. LinkOut - more resources. Full Text Sources. *Elsevier Science. *ClinicalKey ... Impact of beta blockade therapy on long-term mortality after ST-segment elevation acute myocardial infarction in the ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/23228922?dopt=Abstract
  • Synonyms : 1-p-Carbamoylmethylphenoxy-3-isopropylamino-2-propanol, 2-(p-(2-Hydroxy-3-(isopropylamino)propoxy)phenyl)acetamide, 4-(2-Hydroxy-3-((1-methylethyl)amino)propoxy)benzeneacetamide, Atenololum Status : approved Antihypertensive Agents BETA BLOCKING AGENTS CARDIOVASCULAR SYSTEM BETA BLOCKING AGENTS BETA BLOCKING AGENTS Adrenergic beta-1 Receptor Antagonists A cardioselective beta-adrenergic blocker possessing properties and potency similar to propranolol, but without a negative inotropic effect. (pharmakb.com)
  • This reduction in QTc derived entirely from a decrease in the QTc among patients with a baseline abnormal QTc, in whom the shortening in the QTc was greater with propranolol than with either nadolol or metoprolol (p=0.04) since the change in QTc was comparable in all three beta blocker groups with a normal or borderline baseline QTc (p=0.8). (acc.org)
  • Clinical pharmacology studies have demonstrated beta-blocking activity by showing (1) reduction in heart rate and cardiac output at rest and on exercise, (2) reduction of systolic and diastolic blood pressure at rest and on exercise, (3) inhibition of isoproterenol-induced tachycardia, and (4) reduction of reflex orthostatic tachycardia. (pharmacycode.com)
  • The recommended dosage depends on the type, strength, and form of beta blocker and the condition for which it is prescribed. (encyclopedia.com)
  • Labetalol is an alpha-1 and beta adrenergic blocker used to treat high blood pressure. (pharmacycode.com)
  • Beta Blocker (e.g. (fpnotebook.com)
  • Use of calcium antagonist plus beta-blocker may unpredictably cause serious hemodynamic events, marked suppression of sinus node activity, and prolongation of atrioventricular conduction in some patients. (biomedsearch.com)
  • Preoperative beta blocker use associated with cerebral ischemia during carotid endarterectomy. (curehunter.com)
  • P = 0.005) for the association between use of a beta blocker and shunting. (curehunter.com)
  • Although a number of approaches (e.g., beta blockers, permanent pacing, left cervicothoracic sympathectomy, ICD implantation) have been proposed as therapeutic options for patients with the congenital long QT syndromes (LQTS), beta blocker therapy has served as the mainstay of treatment for the majority of these patients. (acc.org)
  • 1-4 Furthermore, the published guidelines recommended an ICD only for LQTS patients who experience syncope or VT while taking a beta blocker (class IIa indication, level of evidence B). 5 However, there is a paucity of data on both the differential electrophysiological and clinical effects of the available beta blockers. (acc.org)
  • In follow-up, the risk reduction for a BCE was correlated with greater QTc shortening on beta blocker therapy. (acc.org)
  • Nadolol has no intrinsic sympathomimetic activity and, unlike some other beta-adrenergic blocking agents, nadolol has little direct myocardial depressant activity and does not have an anesthetic-like membrane-stabilizing action. (pharmacycode.com)
  • Equally, the similarity in the symptomatic, circulatory, and electrocardiographic response to the intravenous and oral preparations suggests that metabolic breakdown products are probably of therapeutic importance only in so far as they antagonize beta-receptor activity. (bmj.com)
  • Twelve replicate wells contained a known agonist, isoproterenol, and four replicate wells contai ned a known antagonist, alprenolol, each diluted in 0.01% DMSO. (bio-medicine.org)
  • Although cardiac failure rarely occurs in properly selected patients, patients being treated with beta-adrenergic blocking agents should be advised to consult the physician at the first sign or symptom of impending failure. (pharmacycode.com)
  • Cardiovascular adverse drug reaction associated with combined beta-adrenergic and calcium entry-blocking agents. (biomedsearch.com)