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.
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.
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.
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.
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.
Drugs that bind to but do not activate excitatory amino acid receptors, thereby blocking the actions of agonists.
Compounds that inhibit or block the activity of NEUROKININ-1 RECEPTORS.
A ligand that binds to but fails to activate the INTERLEUKIN 1 RECEPTOR. It plays an inhibitory role in the regulation of INFLAMMATION and FEVER. Several isoforms of the protein exist due to multiple ALTERNATIVE SPLICING of its mRNA.
Agents inhibiting the effect of narcotics on the central nervous system.
The relationship between the dose of an administered drug and the response of the organism to the drug.
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.
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.
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.
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.
Drugs that bind to but do not activate GABA RECEPTORS, thereby blocking the actions of endogenous GAMMA-AMINOBUTYRIC ACID and GABA RECEPTOR AGONISTS.
Drugs that bind to nicotinic cholinergic receptors (RECEPTORS, NICOTINIC) and block the actions of acetylcholine or cholinergic agonists. Nicotinic antagonists block synaptic transmission at autonomic ganglia, the skeletal neuromuscular junction, and at central nervous system nicotinic synapses.
Drugs that 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.
A family of hexahydropyridines.
Compounds that bind to and block the stimulation of PURINERGIC P1 RECEPTORS.
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 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.
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.
Compounds that selectively bind to and block the activation of ADENOSINE A2 RECEPTORS.
Compounds that bind to and block the stimulation of PURINERGIC P2 RECEPTORS.
Drugs that bind to and block the activation of ADRENERGIC ALPHA-1 RECEPTORS.
Drugs that bind to but do not activate SEROTONIN 5-HT3 RECEPTORS, thereby blocking the actions of SEROTONIN or SEROTONIN 5-HT3 RECEPTOR AGONISTS.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
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.
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.
Compounds that bind to and block the stimulation of ADENOSINE A1 RECEPTORS.
A class of drugs designed to prevent leukotriene synthesis or activity by blocking binding at the receptor level.
Established cell cultures that have the potential to propagate indefinitely.
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.
Agents that antagonize ANGIOTENSIN RECEPTORS. Many drugs in this class specifically target the ANGIOTENSIN TYPE 1 RECEPTOR.
Drugs that bind to but do not activate ADRENERGIC RECEPTORS. Adrenergic antagonists block the actions of the endogenous adrenergic transmitters EPINEPHRINE and NOREPINEPHRINE.
A soluble factor produced by MONOCYTES; MACROPHAGES, and other cells which activates T-lymphocytes and potentiates their response to mitogens or antigens. Interleukin-1 is a general term refers to either of the two distinct proteins, INTERLEUKIN-1ALPHA and INTERLEUKIN-1BETA. The biological effects of IL-1 include the ability to replace macrophage requirements for T-cell activation.
A 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.
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.
Drugs that bind to but do not activate GABA-A RECEPTORS thereby blocking the actions of endogenous or exogenous GABA-A RECEPTOR AGONISTS.
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.
Drugs that bind to and block the activation of ADRENERGIC ALPHA-2 RECEPTORS.
Quantitative determination of receptor (binding) proteins in body fluids or tissue using radioactively labeled binding reagents (e.g., antibodies, intracellular receptors, plasma binders).
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.
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.
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.
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 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 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.
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.
AMINO ALCOHOLS containing the propanolamine (NH2CH2CHOHCH2) group and its derivatives.
Drugs that selectively bind to but do not activate HISTAMINE H3 RECEPTORS. They have been used to correct SLEEP WAKE DISORDERS and MEMORY DISORDERS.
A 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.
Compounds with a six membered aromatic ring containing NITROGEN. The saturated version is PIPERIDINES.
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.
Elements of limited time intervals, contributing to particular results or situations.
Drugs that selectively bind to and activate beta-adrenergic receptors.
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)
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.
Cell surface proteins that bind ENDOTHELINS with high affinity and trigger intracellular changes which influence the behavior of cells.
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.
The rate dynamics in chemical or physical systems.
Drugs that bind to and block the activation of ADRENERGIC BETA-2 RECEPTORS.
A class of drugs that act by selective inhibition of calcium influx through cellular membranes.
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.
Peptides composed of between two and twelve amino acids.
Proteins prepared by recombinant DNA technology.
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.
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.
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.
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.
The parts of a macromolecule that directly participate in its specific combination with another molecule.
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.
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.
Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.
The action of a drug that may affect the activity, metabolism, or toxicity of another drug.
Compounds which inhibit or antagonize the action or biosynthesis of estrogenic compounds.
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.
Compounds with BENZENE fused to AZEPINES.
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)
A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.
Compounds that selectively bind to and block the activation of ADENOSINE A3 RECEPTORS.
A group of compounds that contain the structure SO2NH2.
Glycoproteins which contain sialic acid as one of their carbohydrates. They are often found on or in the cell or tissue membranes and participate in a variety of biological activities.
A 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.
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.
A subtype of endothelin receptor found predominantly in the VASCULAR SMOOTH MUSCLE. It has a high affinity for ENDOTHELIN-1 and ENDOTHELIN-2.
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.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
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 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).
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.
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.
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.
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.
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.
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.
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.
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.
Purine bases found in body tissues and fluids and in some plants.
Compounds that bind to and block the stimulation of PURINERGIC P2X RECEPTORS. Included under this heading are antagonists for specific P2X receptor subtypes.
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.
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.
A specific opiate antagonist that has no agonist activity. It is a competitive antagonist at mu, delta, and kappa opioid receptors.
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.
Seven membered heterocyclic rings containing a NITROGEN atom.
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.
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.
Drugs that bind to and block the activation of PURINERGIC RECEPTORS.
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.
Use of electric potential or currents to elicit biological responses.
The observable response an animal makes to any situation.
Adherence of cells to surfaces or to other cells.
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.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
Compounds bind to and activate ADRENERGIC BETA-2 RECEPTORS.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
An 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.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
Compounds that inhibit or block the activity of CANNABINOID RECEPTORS.
The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.
A class of cell surface receptors for TACHYKININS with a preference for SUBSTANCE P. Neurokinin-1 (NK-1) receptors have been cloned and are members of the G protein coupled receptor superfamily. They are found on many cell types including central and peripheral neurons, smooth muscle cells, acinar cells, endothelial cells, fibroblasts, and immune cells.
A 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.
Compounds that inhibit the action of prostaglandins.
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.
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.
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)
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.
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.
A nucleoside that is composed of ADENINE and D-RIBOSE. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter.
A plant alkaloid with alpha-2-adrenergic blocking activity. Yohimbine has been used as a mydriatic and in the treatment of ERECTILE DYSFUNCTION.
Drugs that bind to and block the activation of MINERALOCORTICOID RECEPTORS by MINERALOCORTICOIDS such as ALDOSTERONE.
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 into the cerebral ventricles.
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.
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.
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)
Drugs that bind to but do not activate GABA-B RECEPTORS thereby blocking the actions of endogenous or exogenous GABA-B RECEPTOR AGONISTS.
A selective serotonin receptor antagonist with weak adrenergic receptor blocking properties. The drug is effective in lowering blood pressure in essential hypertension. It also inhibits platelet aggregation. It is well tolerated and is particularly effective in older patients.
A subclass of cannabinoid receptor found primarily on central and peripheral NEURONS where it may play a role modulating NEUROTRANSMITTER release.
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.
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.
The largest family of cell surface receptors involved in SIGNAL TRANSDUCTION. They share a common structure and signal through HETEROTRIMERIC G-PROTEINS.
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.
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)
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.
A 21-amino acid peptide produced in a variety of tissues including endothelial and vascular smooth-muscle cells, neurons and astrocytes in the central nervous system, and endometrial cells. It acts as a modulator of vasomotor tone, cell proliferation, and hormone production. (N Eng J Med 1995;333(6):356-63)
A subtype of endothelin receptor found predominantly in the KIDNEY. It may play a role in reducing systemic ENDOTHELIN levels.
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.
An amino acid that, as the D-isomer, is the defining agonist for the NMDA receptor subtype of glutamate receptors (RECEPTORS, NMDA).
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.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
Models used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.
Drugs that bind to but do not activate CHOLINERGIC RECEPTORS, thereby blocking the actions of ACETYLCHOLINE or cholinergic agonists.
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.
An alkylamide found in CAPSICUM that acts at TRPV CATION CHANNELS.
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.
An isoquinoline alkaloid obtained from Dicentra cucullaria and other plants. It is a competitive antagonist for GABA-A receptors.
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.
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.
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).
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.
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.
Brain waves with frequency between 15-30 Hz seen on EEG during wakefulness and mental activity.
An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.
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.
A non-essential amino acid naturally occurring in the L-form. Glutamic acid is the most common excitatory neurotransmitter in the CENTRAL NERVOUS SYSTEM.
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.
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.
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.
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)
Compounds with a BENZENE fused to IMIDAZOLES.
Drugs that bind to and block the activation of ADRENERGIC BETA-3 RECEPTORS.
Drugs that bind to and block the activation of ADRENERGIC BETA-1 RECEPTORS.
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.
The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.
Cell surface receptors that are specific for INTERLEUKIN-1. Included under this heading are signaling receptors, non-signaling receptors and accessory proteins required for receptor signaling. Signaling from interleukin-1 receptors occurs via interaction with SIGNAL TRANSDUCING ADAPTOR PROTEINS such as MYELOID DIFFERENTIATION FACTOR 88.
Drugs that selectively bind to and activate alpha adrenergic receptors.
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.
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.
The communication from a NEURON to a target (neuron, muscle, or secretory cell) across a SYNAPSE. In chemical synaptic transmission, the presynaptic neuron releases a NEUROTRANSMITTER that diffuses across the synaptic cleft and binds to specific synaptic receptors, activating them. The activated receptors modulate specific ion channels and/or second-messenger systems in the postsynaptic cell. In electrical synaptic transmission, electrical signals are communicated as an ionic current flow across ELECTRICAL SYNAPSES.
A cell line derived from cultured tumor cells.
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.
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.
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)
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.
The most common inhibitory neurotransmitter in the central nervous system.
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.
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).
A DNA repair enzyme that catalyzes DNA synthesis during base excision DNA repair. EC
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.

Cardiac sympathetic activity estimated by 123I-MIBG myocardial imaging in patients with dilated cardiomyopathy after beta-blocker or angiotensin-converting enzyme inhibitor therapy. (1/4656)

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)

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

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)

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

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)

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

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)

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. (5/4656)

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)

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

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)

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

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)

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

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)

Fingerprint Dive into the research topics of Effects of cardiac rehabilitation and beta-blocker therapy on heart rate variability after first acute myocardial infarction. Together they form a unique fingerprint. ...
There was also no difference in the incidence of the primary endpoint among patients with CAD without a history of MI (12.94 percent vs. 13.55 percent, respectively; p = 0.31). In the cohort of patients only with CAD risk factors, the primary endpoint occurred more frequently among those taking beta-blockers (14.22 percent vs. 12.11 percent, p = 0.02).. Among patients enrolled in the international REACH registry, beta-blocker use was not associated with a lower event rate of cardiovascular events at 44-month follow-up, even among patients with prior history of MI, the study authors concluded. They suggest further research is warranted to identify subgroups that benefit from beta-blocker therapy and the optimal duration of beta-blocker therapy.. ...
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, ...
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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 ...
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.
Source: Can you eat bananas with beta-blockers? At certain times, yes, you can eat bananas even when taking beta-blockers. However, too much potassium can lead to kidney failure and inconsistent heart rhythm. Thus, your doctor may advise and recommend that you restrict your consumption of bananas if you are taking a beta-blocker. The limitation goes with other high-potassium foods, including tomato, papaya, kale, and avocado.. How long can you stay on beta-blockers? Propranolol is usually taken short-term for anxiety medication. That is because its main purpose is to help with physical symptoms. It reduces heart rate and blood pressure, which improves blood flow and eases the workload on your heart. Though there has never been an issue with taking it for too long, you still need to consult your doctor about the risks and benefits of taking it for an extended period. Remember, its best to take the beta blocker only for as long as you need it.. What are the long-term side effects of ...
Dive into the research topics of Current role of beta-adrenergic blockers in the management of chronic heart failure. Together they form a unique fingerprint. ...
The percentage of patients 18 years of age and older during the measurement year who were hospitalized and discharged from July 1 of the year prior to the measurement year to June 30 of the measurement year with a diagnosis of acute myocardial infarction (AMI) and who were prescribed persistent beta-blocker treatment for six months after discharge
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 ...
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
MONDAY, July 13, 2020 (HealthDay News) -- Millions of Americans are prescribed blood pressure medicines called beta blockers, especially after a heart attack. But a new Italian study finds that these go-to drugs might not work as well for women as they do for men.. What we found presents a solid case for reexamination of the use of beta blocker therapy for women with hypertension, said study lead author Dr. Raffaele Bugiardini, professor of cardiology at the University of Bologna.. The study couldnt prove a cause-and-effect link, but among patients taking beta blockers, women had a 4.6% higher rate of heart failure than men when going to the hospital with a heart attack or chest pain (angina), the study found.. For women who have no history of cardiovascular disease and only hypertension, we think it is incredibly important for them to regulate their blood pressure through diet and exercise [first], Bugiardini said in a news release from the journal Hypertension. His team published 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.
This study addressed the question of when and in whom TNF blocker drugs can be stopped. Guidelines are available on when to start TNF blocker therapy and how to induce remission,18 but there is little information regarding patient management once remission is achieved. For most patients, current practice is to continue treatment indefinitely and to stop only for adverse events or secondary non-response. This study assessed clinical, imaging and immunological measures to establish what happens when successful cessation of TNF blockade therapy is achieved. Importantly, our data are the first to show that successful cessation of TNF blocker therapy is more likely if combination therapy is used as first-line treatment. The low levels of inflammation on ultrasound in these patients provided insufficient variance to be associated with outcome. Immunological findings strongly suggest that a state of immunological suppression of inflammation could be associated with sustained remission when patients ...
Beta Blockers - MedHelps Beta Blockers Center for Information, Symptoms, Resources, Treatments and Tools for Beta Blockers. Find Beta Blockers information, treatments for Beta Blockers and Beta Blockers symptoms.
And in a separate look at 30 patients with high blood pressure, they found that people on beta-blockers generally burned fewer calories and fat after a meal - measured by a device called a calorimeter. The patients on beta blockers also reported lower physical activity levels in their day-to-day lives ...
20 double-blind RCTs evaluated the BP lowering efficacy of beta-blockers as second-line drug in 3744 hypertensive patients (baseline BP of 158/102 mmHg; mean duration of 7 weeks). The BP reduction from adding a beta-blocker as the second drug was estimated by comparing the difference in BP reduction between the combination and monotherapy groups. A reduction in BP was seen with adding a beta-blocker to thiazide diuretics or calcium channel blockers at doses as low as 0.25 times the manufacturers recommended starting dose. The BP lowering efficacy of beta-blockers as a second drug was 6/4 mmHg at 1 times the starting dose and 8/6 mmHg at 2 times the starting dose. Beta-blockers reduced heart rate by 10 beats/min at 1 to 2 times the starting dose. Beta-blockers did not statistically significantly increase withdrawals due to adverse effects but this was likely due to the lack of reporting of this outcome in 35% of the included RCTs.. ...
Synonyms for beta-adrenergic blocking agent in Free Thesaurus. Antonyms for beta-adrenergic blocking agent. 3 synonyms for beta-adrenergic blocking agent: beta blocker, beta-adrenergic blocker, beta-blocking agent. What are synonyms for beta-adrenergic blocking agent?
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 ...
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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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. My Views: Of course, your care provider must help you weigh the benefits and risks…
This was a retrospective study, which means the data for it came from previously treated patients, but it was reasonably large (722 patients, of whom 155 were taking beta blockers). So, while this is solid evidence its not the same as a randomised clinical trial. There are lots of questions still to be explored, for example does the effect of beta blockers depend on prior exposure (i.e. do you have to have been taken them for a long time before diagnosis), is the effect still there if beta blockers are started after diagnosis, and at what dosage ...
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 meta-analysis, one that excludes the largely discredited DECREASE studies conducted by disgraced researcher Dr Don Poldermans, suggests that beta-blocker use during noncardiac surgery is killing patients.
Ive been taking beta-blockers, propranolol and then atenolol, for palpitations for years. They dont make me dizzy, and don...
Limitations of the study included the lack of patients with milder forms of COPD airflow obstruction or exacerbation risk, and of course, the trials early end limiting the outcomes. Additionally, investigators had not enrolled patients with a proven indication of beta-blocker use or a prior history with the drug ...
The CSM has advised that beta-blockers, including those considered to be cardioselective, should not be given to patients with a history of asthma or bronchospasm. However, in rare situations where there is no alternative a cardioselective beta-blocker may be used with extreme caution under specialist supervision. Combination preparations containing a beta-blocker are not recommended as they lack flexibility and may not be available in dose combinations appropriate for individual patients ...
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
Beta blockers are used to treat certain types of heart-related problems. Learn about the benefits of using beta blockers from Discovery Health.
Beta blockers are great for treating anxiety and heart conditions, but there are things you should know before you consider trying them.
In a hopeful development, researchers at City of Hope have found that beta-blockers, a common medication used to treat high blood pressure, may be one answer to stopping cancer growth from stress - particularly brain metastases caused from breast cancer.
Nebivolol, (bystolic, nebilet, nebil) is a long acting cardioselective beta-blocker at present approved for the therapy of high blood pressure. Nebivolol is
Beta-adrenergic receptor blockers have been studied for minimizing the effects of catecholamines by blocking their activation of beta receptors. They are used to prevent or treat hypertensive crises, tachycardia, ischemic cardiomyopathy, and arrhythmias. Several studies have shown the efficacy of such drugs in decreasing postoperative morbidity and mortality. This study aimed to evaluate the benefit of perioperative beta-blocker therapy in improving the outcome of CABG surgery regarding intra- and postoperative arrhythmias and ventricular function. It was a prospective controlled nonrandomized study conducted on 50 patients undergoing elective CABG in Ain Shams University hospitals, in which the study group, who were the patients who were compliant on beta-blocker therapy, received 1 mg of propranolol before removal of aortic cross clamp and continued on beta-blocker therapy in the postoperative period, while the control group who were not on beta-blocker therapy received an equivalent volume of normal
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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 ...
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Fingerprint Dive into the research topics of Effect of beta-blocker therapy on heart rate response in patients with hypertension and newly diagnosed untreated obstructive sleep apnea syndrome. Together they form a unique fingerprint. ...
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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, ...
Beta blockers have been proven to have benefit in heart failure (HF) patients with regard to morbidity and mortality. However, initiation and uptitration remains a challenge in many patients. Worsening of heart failure, symptomatic hypotension and symptomatic bradycardia all limit up-titration to the target doses that have been shown to have mortality benefits (carvedilol [Coreg] 25 mg bid, metoprolol succinate [Toprol-XL] 200 mg qd) in the large clinical trials (COPERNICUS, MERIT-HF).. It is debated whether the benefit of beta-blockade is solely due to heart rate reduction or more broadly from the cardiac, central and peripheral effects of blocking sympathetic activity. Clearly, there is a remodeling effect on the dilated ventricle. Furthermore, patients with heart rates of 64 bpm or less are rarely begun on beta-blocker therapy. It is not known whether these patients should be given a pacemaker in order to then safely initiate beta-blocker therapy.. It is also clear that isolated right ...
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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 ...
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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. ...
Comparative Effects of Preoperative Angiotensin-converting Enzyme In-hibitor, Statin and Beta-blocker Treatment on Human Internal Mammary Artery Reactivity in Patients with Coronary Artery Disease: A Pilot Study
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Metoprolol Succinate is the name of the medication. It comes in the form of a tablet, and should be taken by mouth. It belongs to a class of medications called Beta Blocker.
Metoprolol Succinate is the name of the medication. It comes in the form of a tablet, and should be taken by mouth. It belongs to a class of medications called Beta Blocker.
Beta-adrenergic receptor antagonists. Class Summary. These inhibit chronotropic, inotropic, and vasodilatory responses to beta- ... Selective beta-1 - adrenergic receptor blocker that decreases automaticity of contractions. Helps to treat cardiac arrhythmias ... Selectively blocks beta-1 receptors with little or no effect on beta-2 types. Atenolol treats cardiac arrhythmias resulting ... Transforming growth factor beta regulates thyroid growth. Role in the pathogenesis of nontoxic goiter. J Clin Invest. 1989 Mar ...
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. ...
Propranolol is a nonselective beta-adrenergic receptor blocking agent. It has been found to relieve exaggerated startle ... Beta-blockers. Class Summary. Beta-blockers such as propranolol are useful in controlling some symptoms of PTSD caused by ... Alpha-1 Receptor Antagonists. Class Summary. Novel pilot studies in combat veterans suggest alpha-1 antagonists have efficacy ... Alpha-2 Adrenergic Agonists. Class Summary. Agents in this class may decrease vasomotor tone and heart rate by stimulating ...
Adrenergic beta-2 Receptor Antagonists * Subject Areas on Research. * A unique mechanism of beta-blocker action: carvedilol ... Beta(2)-adrenergic and several other G protein-coupled receptors in human atrial membranes activate both G(s) and G(i). ... β2- and β3-adrenergic receptors drive COMT-dependent pain by increasing production of nitric oxide and cytokines. ... Design, synthesis, and functional assessment of Cmpd-15 derivatives as negative allosteric modulators for the β2-adrenergic ...
Pharmacovigilance study of beta adrenergic receptor antagonists in patients visiting department of medicine of a tertiary care ...
Propranolol is a nonselective beta-adrenergic receptor blocking agent. It has been found to relieve exaggerated startle ... Beta-blockers. Class Summary. Beta-blockers such as propranolol are useful in controlling some symptoms of PTSD caused by ... Alpha-1 Receptor Antagonists. Class Summary. Novel pilot studies in combat veterans suggest alpha-1 antagonists have efficacy ... Alpha-2 Adrenergic Agonists. Class Summary. Agents in this class may decrease vasomotor tone and heart rate by stimulating ...
Propranolol is a nonselective beta-adrenergic receptor blocking agent. It has been found to relieve exaggerated startle ... Beta-blockers. Class Summary. Beta-blockers such as propranolol are useful in controlling some symptoms of PTSD caused by ... Alpha-1 Receptor Antagonists. Class Summary. Novel pilot studies in combat veterans suggest alpha-1 antagonists have efficacy ... Alpha-2 Adrenergic Agonists. Class Summary. Agents in this class may decrease vasomotor tone and heart rate by stimulating ...
Enhancement of morphine analgesia by a new adrenergic beta receptor antagonist, 1-isopropylamino-3(4-indanoxy)-2-propanol HC1 ( ... Enhancement of morphine analgesia by a new adrenergic beta receptor antagonist, 1-isopropylamino-3(4-indanoxy)-2-propanol HC1 ( ...
Adrenergic beta-Antagonists / therapeutic use* * Adult * Echocardiography, Doppler, Color* * Electrocardiography* * Female * ... By contrast, a subgroup of three patients that were not treated with an anti-β-adrenergic agent showed LV mass increase from ...
Adrenergic beta-Antagonists. Adrenergic Antagonists. Adrenergic Agents. Neurotransmitter Agents. Molecular Mechanisms of ... treatment with systemic beta-blocker, history of bronchial asthma, chronic obstructive pulmonary disease , sinus bradycardia, ...
Did you mean topic:"adrenergic beta-antagonist - therapeutic use"? Also try beth, or antagonist. ... Adrenergic beta-Antagonists - therapeutic use. Angina Pectoris - drug therapy. Cardiovascular Agents - therapeutic use. ... Mechanisms of angina pectoris -- An overview of treatment and guidelines: ESC/ACC-AHA/NICE -- Beta-blockers -- Calcium channel ...
Beta-adrenergic antagonists (e.g., Propranolol ,160 mg/day). In patients treated with large doses of propranolol (,160 mg/day ... Actions of particular beta-adrenergic antagonists may be impaired when a hypothyroid patient is converted to the euthyroid ...
The current study provides little support for concerns about using beta-blockers (particularly those with vasodilatory actions ... Adrenergic beta-Antagonists / pharmacology * Adrenergic beta-Antagonists / therapeutic use* * Aged * Blood Pressure / drug ... Background: Although beta-blockers reduce the risk of death in CHF, there is little reported experience with these drugs in ... Conclusions: The current study provides little support for concerns about using beta-blockers (particularly those with ...
Adrenergic beta-Antagonists. Adrenergic Antagonists. Adrenergic Agents. Neurotransmitter Agents. Molecular Mechanisms of ... Previous adverse reaction to, or non-compliance with, a beta-blocker. *Current use of medication that may react badly with ...
Beta adrenergic antagonists. *. D. Phosphodiesterase inhibitors. *. 14. Which of the following is the only oral inotropic agent ... You have an African American patient who is intolerant to beta blockers. You know that what combination of medications is very ... This medication is a competitive antagonist of aldosterone at mineralcortioid receptors and reduces mortality in left ... What are the two Beta Blockers approved for treatment of heart failure? ...
Beta-adrenergic antagonists (e.g., Propranolol , 160 mg/day) In patients treated with large doses of propranolol (, 160 mg/day ... Actions of particular beta-adrenergic antagonists may be impaired when a hypothyroid patient is converted to the euthyroid ...
ADRENERGIC BETA-ANTAGONISTS; ADRENERGIC ALPHA-ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; CALCIUM CHANNEL BLOCKERS; ... Antihypertensive agents include diuretics, alpha-adrenergic and beta-adrenergic antagonists, angiotensin-converting enzyme ...
Beta-adrenergic antagonists. Cyclosporine, tacrolimus. Digoxin (acute overdose). Hyperkalemia following acute overdose predicts ... Aldosterone antagonists (spironolactone, eplerenone). Dose-dependent; incidence of hyperkalemia can exceed 20% at higher doses ...
... adrenergic beta-antagonists. Citation: Hakami YA (2015) Transient thyroiditis after surgery for tertiary hyperparathyroidism: a ...
Beta-blockers (beta-adrenergic antagonists): Topical beta-blockers play a large role in PCG treatment and include timolol (non- ... Latent transforming growth factor-beta (TGF-beta) binding proteins: orchestrators of TGF-beta availability. J Biol Chem. 2005; ... Combination beta-blocker/alpha-2 adrenergic agonists: Timolol 0.5%-brimonidine 0.2% (Combigan) must not be prescribed to ... Beta-blockers should be avoided in patients with bradycardia, second- or third-degree atrioventricular block, and active asthma ...
... beta-adrenergic antagonists may be impaired when hypothyroid patient is converted to the euthyroid state ... Beta blockers: Large doses of propranolol (>160 mg/day), T3 and T4 levels change slightly, TSH levels remain normal, and ...
A widely used non-cardioselective beta-adrenergic antagonist. Propranolol has been used for MYOCARDIAL INFARCTION; ARRHYTHMIA; ...
Beta-Blockers. Beta-adrenergic receptor antagonists (beta-blockers) and formoterol may inhibit the effect of each other when ... Although beta2 -receptors are the predominant adrenergic receptors in bronchial smooth muscle and beta1 -receptors are the ... Excessive Use And Use With Other Long-Acting Beta2 -Agonists. As with other inhaled beta2 -adrenergic drugs, PERFOROMIST ... The major adverse effects of inhaled beta2 -agonists occur as a result of excessive activation of the systemic beta-adrenergic ...
A carcinogenicity study in mice of a beta-adrenergic antagonist, primidolol; increased total tumour incidence without tissue ...
ADRENERGIC BETA-ANTAGONISTS are commonly used in the symptomatic treatment of anxiety but are not included here.. ...
insulin deficiency, beta-adrenergic antagonists, acidosis, hyperosmolarity, digitalis, cell lysis. Term. causes of hypokalemia ...
Nielson, K.A., & Jensen, R.A. (1994). Beta-adrenergic receptor antagonist antihypertensive medications impair arousal-induced ...
... long-acting beta-2 adrenergic/long-acting muscarinic antagonist; pMDI: pressurized metered-dose inhaler; inh: inhalation. ... LABD can be beta-2 adrenergics (LABA, long-acting beta-agonists) or anticholinergics (LAMA, long-acting muscarinic antagonists ... LABA/ICS: long-acting beta-2 adrenergic/inhaled corticosteroid; LABA/LAMA: ... SABD can be of 2 types: anti-cholinergics (SAMA, short-acting muscarinic antagonists) such as ipratropium bromide, and short- ...
A later meta-analysis and critical review concluded that beta-adrenergic antagonists are safe in patients with PAD, except in ... The use of beta blockers in patients with intermittent claudication was of concern because several early case reports ...
  • Selectively blocks beta-1 receptors with little or no effect on beta-2 types. (
  • A Beta-2 adrenergic antagonist (β2-adrenoceptor antagonist) is an adrenergic antagonist which blocks the beta-2 adrenergic receptors of cells, with either high specificity (an antagonist which is selective for β2 adrenoceptors) like Butaxamine and ICI-118,551, or non-specifically (an antagonist for β2 and for β1 or β3 adrenoceptors) like the non-selective betablocker Propranolol. (
  • Alprenolol non-selectively blocks beta-1 adrenergic receptors mainly in the heart, inhibiting the effects of epinephrine and norepinephrine resulting in a decrease in heart rate and blood pressure. (
  • Also, with a more minor effect, by binding beta-2 receptors in the juxtaglomerular apparatus, alprenolol inhibits the production of renin, thereby inhibiting angiotensin II and aldosterone production and therefore inhibits the vasoconstriction and water retention due to angiotensin II and aldosterone, respectively. (
  • The effects of beta(3)-adrenoceptor agonist CL-316,243 on adiponectin, adiponectin receptors and tumor necrosis factor-alpha expressions in adipose tissues of obese diabetic KKAy mice. (
  • Albuterol is a sympathomimetic that is selective for beta-2 adrenergic receptors. (
  • It relaxes smooth muscles of the bronchial tree and peripheral vasculature by stimulating adrenergic receptors of the sympathetic nervous system. (
  • BACKGROUND: β-adrenergic receptors are upregulated in melanoma cells and contribute to an immunosuppressive, pro-tumorigenic microenvironment. (
  • Propranolol HCl (AY-64043, ICI-45520, NCS-91523) is a competitive non-selective beta-adrenergic receptors inhibitor with IC50 of 12 nM. (
  • Beta-blockers antagonize beta-adrenergic receptors and are used mainly in the treatment of hypertension, heart failure, tachydysrhythmias. (
  • The drug adheres to the beta-2-adrenergeic receptors in order to relax smooth muscles of the airways to expand the bronchioles for easy flow of air into the lungs. (
  • Adrenalin is a hormone and acts on beta receptors of heart muscles and there by cause stimulation and result in to increase in hear rate and contraction of blood vessels, and result in dialation of air way. (
  • Propranolo is a beta blocker drug its molecular similarity to adrenalin at secondary amine and 2-hydroxy group( iso propyl amino) on the molecule is at naphthyloxy group , make it structurally and stereochemicaly fit for competitive blocking of beta receptors on heart .Its napthyl hydroxyl ring contributes to membrane stabilizing effect. (
  • Naltrexone administered i.t. as a pretreatment reversed the spinal antinociceptive action of beta-endorphin, suggesting that the opioid interacts directly with spinal opiate receptors. (
  • The importance of adrenergic beta 3 receptors on gastro intestinal motility has already been documented. (
  • OBJECTIVE: To determine the metabolic and cardiovascular interaction of beta-adrenergic receptors and ANP. (
  • ANP induced changes in lipid mobilization and glycolysis are mediated by another mechanism, presumably stimulation of natriuretic peptide receptors whereas substrate oxidation might be modulated through adrenergic mechanisms. (
  • Although the order of the alpha1-adrenergic competition seemed to be rather typical for the alpha1B-adrenergic receptors, a molecular analysis on adrenoceptor mRNAs should be made to confirm the exact alpha1-adrenergic subtypes at the level of brown adipocytes, since the possibility of a mixture of different receptor subtypes in brown fat cells and/or tissue may interact with the pharmacological characterization. (
  • Tracers of sympathetic neuronal integrity, b) tracers of adrenergic receptors (11C-CGP12177, 11C-CGP 12388: 11C-GB 67).and c) tracers of the parasympathetic nervous system. (
  • Acebutolol is a beta adrenoceptor antagonist which is cardioselective, i.e. acts preferentially on beta-1 adrenergic receptors in the heart. (
  • They have been shown to reduce the production of melatonin via specific inhibition of beta-1 adrenergic receptors. (
  • Yohimbine, being an antagonist of alpha-2 receptors can shift the balance of sympathetic activity to a place that measurably stimulates lypolisis. (
  • α1-adrenoceptor antagonists cause vasodilation by blocking the binding of norepinephrine to the smooth muscle receptors. (
  • The alpha-1 adrenergic receptor antagonists (also called alpha-blockers) are a family of agents that bind to and inhibit type 1 alpha-adrenergic receptors and thus inhibit smooth muscle contraction. (
  • beta 1-blockers with beta 2 agonist activity are vasodilatory because they activate postsynaptic beta 2 receptors on vascular smooth muscle cell membranes, via the formation of cyclic AMP. (
  • Respiratory anticholinergics are long-acting muscarinic antagonists (LAMA), which relax airway smooth muscles and reduce mucus secretion by blocking muscarinic receptors on the bronchial smooth muscles and the exocrine gland cells in the bronchial passage. (
  • LABAs enhance the activity of beta-2 adrenergic receptors which are stimulated by epinephrine , a natural hormone in the body. (
  • Stimulation of beta-2 receptors results in intracellular action that relaxes bronchial muscles and inhibits hypersensitivity reaction from mast cells, a type of immune cells that initiate allergic reactions. (
  • Activation of beta adrenergic receptors may also induce defensive withdrawal. (
  • The pharmacologic effects of albuterol sulfate are attributable to activation of beta 2 -adrenergic receptors on airway smooth muscle. (
  • Activation of beta 2 -adrenergic receptors leads to the activation of adenylcyclase and to an increase in the intracellular concentration of cyclic-3′,5'‑adenosine monophosphate (cyclic AMP). (
  • While it is recognized that beta 2 -adrenergic receptors are the predominant receptors on bronchial smooth muscle, data indicate that there are beta-receptors in the human heart, 10% to 50% of which are cardiac beta 2 -adrenergic receptors. (
  • Idazoxan hydrochloride (RX 781094 hydrochloride) is an α 2 -adrenoceptor antagonist and is also a imidazoline receptors (IRs) antagonist competitively antagonized the centrally induced hypotensive effect of imidazoline-like drugs (IMs). (
  • Distinctions in the DNA sequence of the genes pertaining to α and β adrenergic receptors can result in genetic polymorphisms. (
  • Given that adrenoreceptors play a fundamental role in regards to the pharmacogenetic interaction between catecholamines with α and β adrenergic receptors, it is, therefore, pivotal to highlight and further analyze variants amongst adrenergic receptors to improve the management of diseases pertaining to catecholamine dysfunction. (
  • In this review, we highlight the pharmacogenomics of adrenergic receptors and their potential clinical implications in critical care. (
  • It is evident that there are several variants associated with the adrenergic receptor alpha 1A (ADRA1A), adrenergic receptor alpha 2A (ADRA2A), adrenergic receptor beta-1 (ADRB1), adrenergic receptor beta-2 genes for α and β adrenergic receptors that were observed among different populations and ethnic groups including the Arg347Cys and Arg389Gly in ADRA1A and ADRB1, respectively. (
  • These polymorphisms have resulted in interindividual variability in drug responses for epinephrine, dexmedetomidine, and salbutamol, which concludes that pharmacogenomics of adrenergic receptors have proven immense variability in candidate genes amongst populations that lead to different drug responses. (
  • It has already been proven in several other tumor entities that stress, mediated by catecholamines and the consecutive activation of adrenergic receptors can lead to proliferation, invasion and migration of tumor cells. (
  • Beta-blockers such as propranolol are useful in controlling some symptoms of PTSD caused by hyperarousal. (
  • Propranolol is a nonselective beta-adrenergic receptor blocking agent. (
  • To assess the adrenergic mechanisms responsible for the effect of epinephrine on glucose production and glucose clearance in man, epinephrine (50 ng/kg/min) was infused in the presence and absence of alpha adrenergic (phentolamine) and beta adrenergic (propranolol) antagonists under conditions when plasma glucose, insulin, and glucagon levels were allowed to vary and when they were clamped by a concurrent infusion of glucose, somatostatin, and insulin. (
  • Inderal - Propranolol is a beta-blocker. (
  • Propranolol is a beta blocker drug (beta adrenergic receptor antagonist) which is used to manage angina pectoris. (
  • Beta-adrenergic antagonists such as metoprolol or propranolol are among the drugs most commonly prescribed for the treatment of cardiovascular disease. (
  • METHODS: Healthy volunteers (n = 36) of white ethnic origin, received a single oral dose of the β-adrenoceptor antagonist, propranolol (40 mg), in a randomised, double-blind, parallel group, placebo-controlled, design. (
  • Propranolol belongs to a group of medicines called beta-blockers and is used to treat hypertension, tremors, angina (chest pain), and other heart or circulatory conditions. (
  • Propranolol is a beta-blocker used to treat high blood pressure, irregular heartbeats, shaking (tremors), help with anxiety and other conditions. (
  • by S Gandhi by II Class In re Propranolol Antitrust Litigation, No. 1:2016cv09901 - Document 134 (S.D.N.Y. 2017) case opinion from the Southern District of New York US Federal by P Roullet by KE Holland Learn about propranolol, a beta-blocker. (
  • Propranolol is a non-selective beta adrenergic antagonist used to treat Amneal Pharmaceuticals of New York Llc, 2016-09-19, Not applicable, US US flag. (
  • Long-Acting injectable forms new york: off-duty cops get peak levels and delirium, and his gp how much by PS Rao Inderal (propranolol) is in a group of drugs called beta-blockers. (
  • This medication is a combination of the following drugs:Beta-BlockersThiazide DiureticsPlease see Propranolol Hydrochloride Oral tablet 10mg Drug Medication Dosage information. (
  • Learn about the reported side effects, related class drugs, and how these by KM Lempert by JW Siefferman Aug 15, 2008 Medscape - Hypertension-specific dosing for Inderal, Inderal LA (propranolol), frequency-based adverse effects, comprehensive interactions, by UY Ryo by AP Mansur by JIM Drayer Propranolol, sold under the brand name Inderal among others, is a medication of the beta New York: Springer. (
  • Of those diagnosed, 5,830 people died from injury because of hypoxemia (anxiousness, tachypnea, tachycardia) and differentiate between current and indirectly prevents calcium overload beta-adrenergic an- tagonists (atenolol, propranolol, meto- prolol, etc cialis y antibioticos. (
  • Always treat the manifestations of hyperthyroidism: Propranolol, a beta-adrenergic blocking agent, for cardiac events. (
  • Propranolol inhibits cavernous vascular malformations by β1 adrenergic receptor antagonism in animal models. (
  • Propranolol, a pleiotropic β-adrenergic blocker, has been anecdotally reported to reduce cerebral cavernous malformations (CCMs) in humans. (
  • Silencing of the β1, but not β2, adrenergic receptor mimicked the beneficial effects of propranolol in a zebrafish CCM model, as did the β1-selective antagonist metoprolol. (
  • Thus, propranolol ameliorated cavernous malformations by β1 adrenergic antagonism in zebrafish. (
  • Propranolol or other β1-selective antagonists may be beneficial in CCM disease. (
  • In particular, we used the method of local microinjection into the vermal cortex of the cerebellar anterior lobe of the non-selective beta-adrenergic agonist ((+/-) -isoproterenol hydrochloride) or antagonist (dl-propranolol hydrochloride) to act on both beta 1- and beta 2-adrenoceptors. (
  • Prazosin, clonidine, CDP, l-propranolol and the CRF-antagonist, alpha-helical CRF9-41 (25 micrograms i.c.v.), reversed the restraint-induced increase in the latency and MTIC. (
  • Mechanisms of angina pectoris -- An overview of treatment and guidelines: ESC/ACC-AHA/NICE -- Beta-blockers -- Calcium channel blockers -- Nitrates -- Nicorandil -- Ivabradine -- Trimetazidine -- Ranolazine -- New antianginal drugs still not available for clinical use -- Medical therapy versus revascularization in the management of stable angina pectoris. (
  • Although beta-blockers reduce the risk of death in CHF, there is little reported experience with these drugs in patients with a low pretreatment SBP, who may respond poorly to beta-blockade. (
  • The current study provides little support for concerns about using beta-blockers (particularly those with vasodilatory actions) in patients with severe CHF who have a low SBP. (
  • What are the two Beta Blockers approved for treatment of heart failure? (
  • You have an African American patient who is intolerant to beta blockers. (
  • Antihypertensive agents include diuretics, alpha-adrenergic and beta-adrenergic antagonists, angiotensin-converting enzyme inhibitors, calcium channel blockers, ganglionic blockers, and vasodilator agents. (
  • Sotalol is in a class of medications called antiarrhythmics (beta-blockers). (
  • Use of diuretics, angiotensin converting enzyme (ACE) inhibitors, beta adrenergic receptor antagonists (beta blockers), alpha adrenergic receptor antagonists (alpha blockers), calcium channel blockers (CCBs) etc. are not efficient enough to cure hypertension. (
  • Until now, there are different antihypertensive therapies available, such as: ACE (classified as EC3.4.15.1) inhibitors, angiotensin receptor blocker (ARB), beta blockers, diuretics, and also CCBs [7] [8]. (
  • No important differences are clearly apparent among the benefits of different beta blockers, although some are more convenient than others (or have slightly fewer side effects), and it appears that those with appreciable intrinsic sympathomimetic activity may confer less benefit. (
  • Primary prevention with cardioprotective agents such as dexrazoxane, angiotensin-converting enzyme (ACE) inhibitors, beta-blockers (BBs), or statins cannot be generally recommended due to lack of scientific evidence. (
  • Baseline use of beta-blockers, diuretics and MRAs was similar between men and women, while women had greater use of digitalis and ARBs and less use of ACE inhibitors. (
  • KCNQ1 is regarded by the American College of Medical Genetics (ACMG) as `actionable' since appropriate preventative treatment is available (beta-blockers). (
  • Beta blockers may antagonize albuterol. (
  • For more information, see "Cal-cium channel blockers,") The patient may also receive a beta-adrenergic antagonist, angiotensin-converting enzyme (ACE) inhibitor, or an angiotensin II receptor blocker. (
  • Other drugs used to treat hypertension include sympatholytic drugs (other than beta-adrenergic blockers), and vasodilators. (
  • Beta-blockers can be used alone or concomitantly with other antihypertensive agents. (
  • Protective effects of beta-blockers. (
  • Jul Treatment with calcium salts may provide benefits for hypotensive patients who overdosed on beta-blockers alone or in combination with a calcium. (
  • Poisoning by beta-blockers or CCBs usually produces hypotension and bradycardia, which may be refractory to standard resuscitation measures. (
  • Beta blockers are a commonly used antiarrhythmia medication, which when overdosed can lead to various effects throughout the body such as bradycardia and bronchospasm. (
  • The adverse CV risks posed byhypertension, metabolic syndrome, and diabetescan be substantially reduced throughthe use of angiotensin-converting enzyme(ACE) inhibitors and beta blockers. (
  • Policosanol can exert hypotensive effect, but probability and intensity of clinically significant additive effect with beta blockers are uncertain. (
  • Drugs such as beta-adrenergic antagonists (beta blockers) have been linked to a range of adverse effects, including depression. (
  • While treatment with beta blockers was not found to be associated with an increased incidence of depression, some studies recorded higher levels of sleep disturbance. (
  • We found no evidence to suggest a link between the use of beta blockers and depression," says Prof. Dr. Reinhold Kreutz, Director of Charité's Institute of Clinical Pharmacology and Toxicology. (
  • Continuing his description of the meta-analysis conducted by his team - the first to study the full range of psychiatric side effects - he adds: "However, some patients developed sleep-related symptoms during treatment with beta blockers. (
  • These were taken from 285 individual studies and involved 24 different beta blockers. (
  • Despite being the most commonly reported psychiatric side effect, depression did not occur more frequently during treatment with beta blockers than during treatment with a placebo. (
  • This means that, while we found no causal link for this problem with beta blockers, these patients should be anyway monitored in this regard in clinical practice. (
  • Patients treated with beta blockers were no more likely to discontinue their medications due to depression than patients undergoing different treatments. (
  • Among the other side effects studied - such as anxiety and loss of appetite, memory, or libido - only sleep disturbance and abnormal dreams were found to be linked with beta blockers. (
  • Summing up the results of the research, Prof. Kreutz says: "Our results show that concerns regarding undesirable psychiatric effects, in particular depression, should not influence the decision-making process regarding the use of beta blockers. (
  • For the most part, beta blockers have a good psychiatric safety profile. (
  • Therefore, concerns about psychological health should not affect the clinical use of beta-blockers. (
  • Beta-agonists and beta-blockers are pharmacologic opposites, and will counteract each other to some extent when given concomitantly, especially when non-cardioselective beta blockers how hwo. (
  • 18 studies reported calcium-channel blockers, vasodilators and beta-blockers lowered BP postpartum. (
  • Both beta-adrenergic receptor antagonist drugs (beta-blockers) and non-dihydropyridine calcium-channel blockers (non-DHP CCBs), ie, diltiazem and verapamil, can cause sinus arrest or severe sinus bradycardia, and when drugs from the two classes are used together, these effects may be more than additive. (
  • Calcium channel blockers should be favored over beta blockers in patients with asthma (or other forms of pulmonary disease with a bronchospastic component) given the risk of exacerbating bronchospasm. (
  • Therefore, patients with asthma should not normally be treated with beta-blockers. (
  • In this setting, cardioselective beta-blockers could be considered, although they should be administered with caution. (
  • The activators are called agonists, while the blockers are antagonists. (
  • Beta blockers have long been associated with sleep disturbances such as difficulty falling asleep, staying asleep, and insomnia. (
  • 2. Adrenergic beta blockers, Clonidine, Methyldopa, NSAIDs, Angiotensin-converting enzyme inhibitors, Angiotensin receptor blockers, Renin inhibitors and Dihydropyridine calcium channel antagonists should be discontinued for 2 weeks. (
  • Are beta blockers vasodilators? (
  • Long-acting beta 2 -adrenergic agonists (LABA) increase the risk of asthma-related death. (
  • Drugs with a possible risk for QT prolongation that should be used cautiously and with close monitoring with ofloxacin include the beta-agonists. (
  • The interaction may be less likely with inhaled beta-agonists versus those given systemically. (
  • Agents that prolong the QT interval and that should be used cautiously with prochlorperazine include the beta-agonists. (
  • Minor Beta-agonists should be used cautiously and with close monitoring with anagrelide. (
  • There are several routes by which a medication can be taken: Drugs with a possible risk for QT prolongation that should be used cautiously with maprotiline include the beta-agonists. (
  • Beta-adrenergic receptor blocking agents not only block the pulmonary effect of beta-agonists, such as albuterol tablets, but may produce severe bronchospasm in asthmatic patients. (
  • The ECG changes and/or hypokalemia that may result from the administration of nonpotassium-sparing diuretics (such as loop or thiazide diuretics) can be acutely worsened by beta-agonists, especially when the recommended dose of the beta-agonist is exceeded. (
  • Although the clinical significance of these effects is not known, caution is advised in the coadministration of beta-agonists with nonpotassium-sparing diuretics. (
  • After failure of beta-adrenergic antagonists to control intraocular pressure (iop) despite a long history of beta-adrenergic agonists and a history of previous glaucoma surgery, clomiphene citrate was chosen. (
  • The type II 5'-deiodinase (5'DII) was activated in response to simultaneous stimulation by beta3- and alpha1-adrenergic agonists, BRL 37344 or CGP 12177, and cirazoline, in brown adipocytes. (
  • Because metaproterenol is not brain penetrant - meaning that it can not pass through the protective blood-brain-barrier membrane surrounding the brain - the investigators added six related drugs, including the two selective Beta 2 -Adrenoreceptor agonists, clenbuterol and salbutamol (which are both brain penetrant). (
  • Thus, Beta 2 -Adrenoreceptor agonists are effectively epinephrine. (
  • And what medical conditions are treated with Beta 2 -Adrenoreceptor agonists? (
  • Beta 2 -Adrenoreceptor agonists cause smooth muscle fibres to relax. (
  • Ok, so these researchers found Beta 2 -Adrenoreceptor agonists reduce the production of Alpha Synuclein in their screening experiment? (
  • The cells treated with Beta 2 -Adrenoreceptor agonists generated less of the Parkinson's disease associated protein. (
  • Adrenergic Beta-Agonists - Thera. (
  • These variations can potentially impact response to treatment with adrenergic agonists and antagonists that likely warrant medical intervention. (
  • Short-acting beta-agonists (SABAs) are a class of prescription drugs used to quickly relieve shortness of breath and wheezing in people with asthma. (
  • Short -acting beta-2 agonists (SABAs), such as salbutamol and terbutaline, have a rapid onset of action (15 minutes) and their effects last for up to 4 hours. (
  • Data from a large placebo-controlled US study that compared the safety of another longacting beta 2 -adrenergic agonist (salmeterol) or placebo added to usual asthma therapy showed an increase in asthma-related deaths in patients receiving salmeterol. (
  • Isoprenaline HCl (NCI-c55630,Isoproterenol hydrochloride) is a non-selective beta-adrenergic receptor agonist, used for the treatment of bradycardia and heart block. (
  • Clonidine, an alpha-2 adrenergic agonist, is a frequent premedication. (
  • A short-acting beta-2 adrenergic agonist that is primarily used as a bronchodilator agent to treat ASTHMA. (
  • Weigh the risks of co-use, and where write, allow a washout period after discontinuation of the MAOI before instituring beta-agonist treatment or vice-versa. (
  • Amongst these 35 compounds was the selective Beta 2 -Adrenoreceptor agonist metaproterenol . (
  • Hang on a second, what are Beta 2 -Adrenoreceptor agonist? (
  • Agonist vs antagonist. (
  • Beta 2 -Adrenoreceptor agonist are drugs that bind to and activate the Beta 2 -Adrenergic receptor. (
  • Albuterol sulfate is a beta 2 -adrenergic agonist. (
  • LABA (BRONCHODILATOR) The second medicine is an inhaled long-acting beta2-adrenergic agonist (LABA) called formoterol. (
  • For patients on a long-acting muscarinic antagonist (LAMA), a short-acting beta agonist (SABA) is generally used for quick relief of COPD symptoms. (
  • Background The Global Initiative for Asthma recommends as-needed inhaled corticosteroid (ICS)-formoterol as an alternative to maintenance ICS plus short-acting beta 2-agonist (SABA) reliever at Step 2 of their stepwise treatment algorithm. (
  • Beta blockade during and after myocardial infarction: an overview of the randomized trials. (
  • Long-term beta blockade for perhaps a year or so following discharge after an MI is now of proven value, and for many such patients mortality reductions of about 25% can be achieved. (
  • By contrast, although very early IV short-term beta blockade can definitely limit infarct size, more reliable information about the effects of such treatment on mortality will not be available until a large trial (ISIS) reports later this year, with data on some thousands of patients entered within less than 4 hours of the onset of pain. (
  • When alpha adrenergic blockade was superimposed on beta blockade, the increase in glucose production and the decrease in both plasma insulin and glucose clearance observed during infusion of epinephrine alone was virtually abolished. (
  • In contrast, when plasma glucose, insulin, and glucagon were clamped, beta adrenergic blockade completely prevented the suppression of glucose clearance by epinephrine and inhibited the stimulation of glucose production by epinephrine by 80% whereas alpha adrenergic blockade had no effect on either of these parameters. (
  • Therapeutic responsiveness to vagus nerve stimulation in patients receiving beta-blockade for heart failure with reduced ejection fraction. (
  • Risk-reduction strategies utilising pharmacotherapy with beta blockade and statins have shown the most promise. (
  • This process is initiated by the non-selective beta1 and beta2 adrenergic receptor blockade. (
  • We further investigated the effects of beta-adrenergic and cholinergic receptor blockade on blood flow and heart rate during these activities. (
  • Integrated response to exercise in patients with hypertrophic obstructive cardiomyopathy and effect of beta-adrenergic blockade on oxygen transport. (
  • beta-adrenergic receptor blockade abolished the response. (
  • Schnelle K Clinical pharmacology of adrenergic beta receptor blockade with sotalol (MJ 1999). (
  • GRK5 Gln41Leu polymorphism is not associated with sensitivity to beta(1)-adrenergic blockade in humans. (
  • Dungan, K. W. Pharmacological and toxicological properties of two new β-adrenergic receptor antagonists Journal of Pharmacology and Experimental Therapeutics (1965), 149(2), 161-73. (
  • Formoterol fumarate dihydrate is a beta 2 -adrenergic bronchodilator. (
  • It is essentially a selective beta-2-adrenergic antagonist and a bronchodilator. (
  • This recommendation does not preclude the judicious use of an aerosol bronchodilator of the adrenergic stimulant type in patients receiving albuterol tablets. (
  • Selective beta-1 - adrenergic receptor blocker that decreases automaticity of contractions. (
  • Alprenolol is a non-selective beta-blocker used in the treatment of hypertension, edema, ventricular tachycardias, and atrial fibrillation. (
  • One of the active metabolites, 4-OH-alprenolol, is an active beta-blocker. (
  • If monitored, the side effects of long-term therapy are not a major problem, as when they occur they are easily reversible by changing the beta blocker or by discontinuation of treatment. (
  • Our aim has been not only to review the 65-odd randomized beta blocker trials but also to demonstrate that when many randomized trials have all applied one general approach to treatment, it is often not appropriate to base inference on individual trial results. (
  • Patients were included if they were >18 years old, had NYHA functional class II-IV HF, left ventricular ejection fraction (LVEF) ≤35 percent, elevated natriuretic peptide levels and were taking an angiotensin-converting enzyme (ACE) inhibitor or angiotensin-receptor blocker (ARB), beta-blocker (unless contraindicated or not tolerated) and mineralocorticoid receptor antagonists (MRAs), if indicated. (
  • Levobunolol is an ophthalmic beta-blocker, equally effective at β(1)- and β(2)-receptor sites. (
  • Documentation of medical reason(s) for not prescribing beta-blocker therapy (e.g., low blood pressure, fluid overload, asthma, patients recently treated with an intravenous positive inotropic agent, allergy, intolerance, other medical reasons). (
  • Documentation of patient reason(s) for not prescribing beta-blocker therapy (e.g., patient declined, other patient reasons). (
  • Documentation of system reason(s) for not prescribing beta-blocker therapy (e.g., other reasons attributable to the healthcare system). (
  • Numerator will be populated with patients prescribed a beta-blocker therapy within the measurement period. (
  • However, in beta-blocker poisoning where symptomatic bradycardia and hypotension are present. (
  • Mar 03, · The primary toxicity in a beta blocker overdose is cardiac. (
  • Good supportive care is important, in addition to the first line treatment for beta blocker overdose: high dose glucagon (see below). (
  • Jul 12, · Summarize the treatment and management options available for beta-blocker toxicity. (
  • Outline interprofessional team strategies for improving care coordination and communication to evaluate and treat beta-blocker toxicity and improve outcomes. (
  • Although there have been no controlled trials to prove the efficacy of glucagon in poisoning beta-blocker overdose, glucagon is considered as a useful treatment of choice. (
  • Summarize the treatment and management options available for beta-blocker toxicity. (
  • For cases of beta-blocker poisoning where symptomatic bradycardia and hypotension are present, high-dose glucagon is considered the first-line antidote. (
  • Beta-adrenergic antagonist (ie, beta-blocker) toxicity can produce clinical manifestations including bradycardia, hypotension, arrhythmias. (
  • Although they end in "lol," beta blocker overdoses are no laughing matter. (
  • Since ambulatory blood pressure monitoring in a cross-over trial design can reliably detect differences of 5 mmHg with less than 20 subjects, we have used this technique to assess the dose-response curve of a new beta-blocker, carvedilol. (
  • The judicious use of a cardioselective beta-receptor blocker may be considered, bearing in mind that such medication can produce bronchospasm. (
  • Which is better beta blocker or calcium blocker? (
  • Importance of heart rate in determining beta-blocker efficacy in acute and long-term acute myocardial in farction intervention trials Am J Cardiol 1986;57:43F-49F. (
  • It is a non-selective competitive beta-adrenergic receptor blocker that also exhibits Class III antiarrhythmic properties by its inhibition of potassium channels. (
  • It is a non-selective, β-adrenergic receptor antagonist and an α1-adrenoceptor blocker. (
  • One of the adrenergic beta-antagonists used as an antihypertensive, anti-anginal, and anti-arrhythmic agent. (
  • A beta-adrenergic antagonist used as an anti-arrhythmia agent, an anti-angina agent, an antihypertensive agent, and an antiglaucoma agent. (
  • Phenoxybenzamine is a synthetic, dibenzamine alpha adrenergic antagonist with antihypertensive and vasodilatory properties. (
  • Nonselective, competitive beta-receptor antagonist with no intrinsic sympathetic activity. (
  • A nonselective beta-adrenoceptor antagonist used in the treatment of glaucoma. (
  • As the drug is a nonselective &beta-adrenergic blocking agent, it can produce both systemic pulmonary and cardiovascular effects following topical application to the eye. (
  • Phentolamine Mesylate(Phentolamine methanesulfonate) is a reversible and nonselective alpha-adrenergic receptor antagonist, used for the prevention or control of hypertensive episodes. (
  • Did you mean topic:"adrenergic beta-antagonist - therapeutic use" ? (
  • At therapeutic doses, nebivolol is devoid of alpha-adrenergic antagonism. (
  • Graybug is also using its proprietary technologies to develop GB-401, an injectable depot formulation of a beta-adrenergic prodrug, for primary open angle glaucoma, with a dosing regimen of up to six months, and GB-103, a longer-acting version of GB-102, designed to deliver therapeutic drug levels to the retinal tissue for 12 months with a single injection. (
  • Relationship between systemic and coronary vascular responses to digoxin and concurrent drug therapy with verapamil/beta-adrenoceptor antagonists in humans. (
  • Rodent and human beta 3-adrenergic receptor genes contain an intron within the protein-coding block. (
  • Potent and selective human beta(3)-adrenergic receptor antagonists. (
  • The mechanism for the beta adrenergic effects remains to be defined but may reflect a direct action of epinephrine on hepatic and peripheral tissues. (
  • CONCLUSIONS: Dorzolamide, a carbonic anhydrase inhibitor, has additive effects as an ocular hypotensive agent with timolol, a beta-adrenergic antagonist, even though both drugs are suppressors of aqueous humor flow. (
  • Levobunolol is a beta-adrenergic antagonist used for the reduction of elevated intraocular pressure in patients with ocular hypertension or open-angle glaucoma. (
  • Aviado DM.Sotalol, a pure beta-adrenergic blocking agent for treatment of essential hypertension and other cardiovascular diseases. (
  • 1. In 24 patients who were undergoing coronary arteriography for the assessment of ischaemic heart disease, the relationship between the systemic and coronary vascular responses to acute intravenous digoxin administration (500 micrograms) and concurrent drug therapy with the calcium antagonist verapamil (group I) or a beta-adrenoceptor antagonist (group II) or neither of these agents (group III) was examined. (
  • An update to our 2015 post on HIET for beta-adrenergic receptor and calcium channel antagonists overdose. (
  • 2 β-adrenergic stimulation, which increases during stress states, suppresses NK activity and therefore promotes metastasis. (
  • Our findings illustrate that surfacing is accompanied by an increase in heart rate that is primarily due to beta-adrenergic stimulation. (
  • CONCLUSIONS: Selected cardiovascular ANP effects are at least partly mediated by beta-adrenergic receptor stimulation. (
  • A widely used non-cardioselective beta-adrenergic antagonist. (
  • Levobetaxolol is a cardioselective (beta-1¬ adrenergic) receptor-blocking agent that does not have significant membrane-stabilizing (local anesthetic) activity and is devoid of intrinsic sympathomimetic action. (
  • These inhibit chronotropic, inotropic, and vasodilatory responses to beta-adrenergic activity observed in hyperthyroidism. (
  • Alprenolol has little to no intrinsic sympathomimetic activity and, unlike some other beta-adrenergic blocking agents, alprenolol has little direct myocardial depressant activity and does not have an anesthetic-like membrane-stabilizing action. (
  • However, under certain circumstances, e.g., as prophylaxis after myocardial infarction, there may be no acceptable alternatives to the use of beta-adrenergic blocking agents in patients with asthma. (
  • SPECT techniques with 123 I metaiodobenzylguanidine (MIBG) offer informations about the cardiac sympathetic function but the value for the quantitative assessment of myocardial adrenergic nervous system is limited due to the restricted spatial resolution. (
  • However, methodological problems limit the value of this method for the quantitative assessment of myocardial adrenergic nervous system due to the restricted spatial resolution [5,6]. (
  • β adrenergic receptor antagonists slow the heart rate and decrease the myocardial contractility, these prolongs the systolic conduction and disturbs the ventricular fibres. (
  • With antithyroid drugs, inorganic iodide, corticosteroids and beta-adrenergic antagonists has. (
  • Phentolamine and tolazoline are competitive α adrenergic antagonists and block the receptor for 5-HT and it causes the release of histamine from the mast cells, which is a potent vasodilator. (
  • Nebivolol shows high affinity and selectivity for beta 1-adrenergic receptor sites in a rabbit lung membrane preparation (K i value = 0.9 nM and beta 2/beta 1 ratio = 50). (
  • It is a competitive and selective pi-adrenoceptor antagonist: this effect is attributed to the SRRR-nebivolol (D-nebivolol). (
  • Improving regional/national empirical treatment with one hour or the body from the beta-adrenergic antagonist nebivolol. (
  • Effects of beta-adrenergic blocking agents on specific binding of [3H]D-Ala2-Met5-enkephalinamide and [3H]naloxone. (
  • Dive into the research topics of 'Effects of beta-adrenergic blocking agents on specific binding of [3H]D-Ala2-Met5-enkephalinamide and [3H]naloxone. (
  • An inhibitory effect on tumor growth after treatment with the corresponding antagonists, thus adrenoceptor blocking agents, was also observed. (
  • Spinal administration of the alpha 1-adrenoceptor antagonist WB-4101 failed to alter the analgesic effects of the opioid, whereas the alpha 2-adrenoceptor antagonist yohimbine completely blocked beta-endorphin-induced elevations in tail-flick latency. (
  • Helios contains a blend of clenbuterol hydrochloride and yohimbine hydrochloride, a very potent combination of a beta and alpha antagonist.Clenbuterol and yohimbine promote fat loss through the same adrenergic system, but the effects are through very different mechanisms. (
  • Yohimbine HCL - a powerful stimulant and alpha-2 adrenergic receptor antagonist, shown to increase blood flow to the skin's surface, upper, and lower extremities of the body. (
  • Albuterol acts as a functional antagonist to relax the airway irrespective of the spasmogen involved, thus protecting against all bronchoconstrictor challenges. (
  • The clinical relevance of these haemodynamic differences as compared to other beta-adrenoreceptor antagonists has not been fully established. (
  • The outcomes regiStry for non-vitamin k antagonist oral anticoagUlants treatmeNt in variouS tHrombotIc dIseases for better cliNical practicE (SUNSHINE) is a multicenter, prospective, observational non-interventional inpatient/outpatient disease registry to assess the utilization of Non-vitamin k antagonist oral anticoagulants (NOACs), and associated outcomes. (
  • α -Adrenergic receptor response in clinical relevance include α1 receptor mediated contraction of arterial and venous smooth muscle. (
  • These results indicate that in man, epinephrine increases glucose production and decreases glucose clearance by both alpha and beta adrenergic actions. (
  • Beta 2 -Adrenergic receptor interacts with a chemical called epinephrine, which is a neurotransmitter like dopamine. (
  • Epinephrine will come floating along, bind to the Beta 2 -Adrenergic receptor, and activate it. (
  • Variability in vasomotor responses to digoxin is not clearly related to concurrent drug therapy with verapamil or a beta-adrenoceptor antagonist. (
  • Novel pilot studies in combat veterans suggest alpha-1 antagonists have efficacy on the sleep-associated symptoms of PTSD. (
  • An adrenergic beta-antagonist that is used in the treatment of life-threatening arrhythmias. (
  • The alpha adrenergic effects could be accounted for by inhibition of insulin secretion. (
  • Regarding the tracers of sympathetic neuronal integrity there are two subgroups: 1) radiolabeled endogenous neurotransmitters or true adrenergic neurotransmitters which are molecular identical to endogenous neurotransmitters and they follow the metabolic pathways of catecholamines within the myocardium and sympathetic neurons and 2) radiolabeled catecholamine analogues or false neurotransmitters that are resistant to specific steps of catecholamine degradation, follow the same uptake and release mechanisms, without being metabolized like the endogenous transmitters. (
  • Pharmacological characterization of alpha1- and beta-adrenergic synergism of 5'DII activity in rat brown adipocytes. (
  • Thus, specific alpha1- and beta-adrenoceptor subtypes participate in the regulation of 5'DII activity in the rat brown adipocytes, and therefore, an impaired alpha1- and beta-adrenergic co-work may be involved in a defective BAT function, e.g., in obese Zucker rats, too. (
  • Effect of combined low-dose oral prednisone with beta-adrenergic receptor antagonists for refractory infantile hemangiomas: retrospective cohort study in 76. (
  • beta-Endorphin administered intrathecally (i.t.) in rats produced a dose-dependent elevation in tail-flick latency. (

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