Adrenergic Agents: Drugs that act on adrenergic receptors or affect the life cycle of adrenergic transmitters. Included here are adrenergic agonists and antagonists and agents that affect the synthesis, storage, uptake, metabolism, or release of adrenergic transmitters.Sympathomimetics: Drugs that mimic the effects of stimulating postganglionic adrenergic sympathetic nerves. Included here are drugs that directly stimulate adrenergic receptors and drugs that act indirectly by provoking the release of adrenergic transmitters.Adrenergic Agonists: Drugs that bind to and activate adrenergic receptors.Epinephrine: The active sympathomimetic hormone from the ADRENAL MEDULLA. It stimulates both the alpha- and beta- adrenergic systems, causes systemic VASOCONSTRICTION and gastrointestinal relaxation, stimulates the HEART, and dilates BRONCHI and cerebral vessels. It is used in ASTHMA and CARDIAC FAILURE and to delay absorption of local ANESTHETICS.Phentolamine: A nonselective alpha-adrenergic antagonist. It is used in the treatment of hypertension and hypertensive emergencies, pheochromocytoma, vasospasm of RAYNAUD DISEASE and frostbite, clonidine withdrawal syndrome, impotence, and peripheral vascular disease.Isoproterenol: Isopropyl analog of EPINEPHRINE; beta-sympathomimetic that acts on the heart, bronchi, skeletal muscle, alimentary tract, etc. It is used mainly as bronchodilator and heart stimulant.Propranolol: A widely used non-cardioselective beta-adrenergic antagonist. Propranolol has been used for MYOCARDIAL INFARCTION; ARRHYTHMIA; ANGINA PECTORIS; HYPERTENSION; HYPERTHYROIDISM; MIGRAINE; PHEOCHROMOCYTOMA; and ANXIETY but adverse effects instigate replacement by newer drugs.Receptors, Adrenergic: Cell-surface proteins that bind epinephrine and/or norepinephrine with high affinity and trigger intracellular changes. The two major classes of adrenergic receptors, alpha and beta, were originally discriminated based on their cellular actions but now are distinguished by their relative affinity for characteristic synthetic ligands. Adrenergic receptors may also be classified according to the subtypes of G-proteins with which they bind; this scheme does not respect the alpha-beta distinction.Receptors, Adrenergic, alpha: One of the two major pharmacological subdivisions of adrenergic receptors that were originally defined by the relative potencies of various adrenergic compounds. The alpha receptors were initially described as excitatory receptors that post-junctionally stimulate SMOOTH MUSCLE contraction. However, further analysis has revealed a more complex picture involving several alpha receptor subtypes and their involvement in feedback regulation.Prazosin: A selective adrenergic alpha-1 antagonist used in the treatment of HEART FAILURE; HYPERTENSION; PHEOCHROMOCYTOMA; RAYNAUD DISEASE; PROSTATIC HYPERTROPHY; and URINARY RETENTION.Adrenergic alpha-Agonists: Drugs that selectively bind to and activate alpha adrenergic receptors.Phenylephrine: An alpha-1 adrenergic agonist used as a mydriatic, nasal decongestant, and cardiotonic agent.Adrenergic alpha-Antagonists: Drugs that bind to but do not activate alpha-adrenergic receptors thereby blocking the actions of endogenous or exogenous adrenergic agonists. Adrenergic alpha-antagonists are used in the treatment of hypertension, vasospasm, peripheral vascular disease, shock, and pheochromocytoma.Norepinephrine: Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.Receptors, Adrenergic, beta: One of two major pharmacologically defined classes of adrenergic receptors. The beta adrenergic receptors play an important role in regulating CARDIAC MUSCLE contraction, SMOOTH MUSCLE relaxation, and GLYCOGENOLYSIS.Adrenergic beta-Antagonists: Drugs that bind to but do not activate beta-adrenergic receptors thereby blocking the actions of beta-adrenergic agonists. Adrenergic beta-antagonists are used for treatment of hypertension, cardiac arrhythmias, angina pectoris, glaucoma, migraine headaches, and anxiety.Calcium Channel Blockers: A class of drugs that act by selective inhibition of calcium influx through cellular membranes.Metoprolol: A selective adrenergic beta-1 blocking agent that is commonly used to treat ANGINA PECTORIS; HYPERTENSION; and CARDIAC ARRHYTHMIAS.Propanolamines: AMINO ALCOHOLS containing the propanolamine (NH2CH2CHOHCH2) group and its derivatives.Antihypertensive Agents: Drugs used in the treatment of acute or chronic vascular HYPERTENSION regardless of pharmacological mechanism. Among the antihypertensive agents are DIURETICS; (especially DIURETICS, THIAZIDE); ADRENERGIC BETA-ANTAGONISTS; ADRENERGIC ALPHA-ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; CALCIUM CHANNEL BLOCKERS; GANGLIONIC BLOCKERS; and VASODILATOR AGENTS.Angiotensin-Converting Enzyme Inhibitors: A class of drugs whose main indications are the treatment of hypertension and heart failure. They exert their hemodynamic effect mainly by inhibiting the renin-angiotensin system. They also modulate sympathetic nervous system activity and increase prostaglandin synthesis. They cause mainly vasodilation and mild natriuresis without affecting heart rate and contractility.Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.Coronary Disease: An imbalance between myocardial functional requirements and the capacity of the CORONARY VESSELS to supply sufficient blood flow. It is a form of MYOCARDIAL ISCHEMIA (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels.Lipoproteins: Lipid-protein complexes involved in the transportation and metabolism of lipids in the body. They are spherical particles consisting of a hydrophobic core of TRIGLYCERIDES and CHOLESTEROL ESTERS surrounded by a layer of hydrophilic free CHOLESTEROL; PHOSPHOLIPIDS; and APOLIPOPROTEINS. Lipoproteins are classified by their varying buoyant density and sizes.Terminology as Topic: The terms, expressions, designations, or symbols used in a particular science, discipline, or specialized subject area.Atherosclerosis: A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.Cholesterol, HDL: Cholesterol which is contained in or bound to high-density lipoproteins (HDL), including CHOLESTEROL ESTERS and free cholesterol.Adverse Drug Reaction Reporting Systems: Systems developed for collecting reports from government agencies, manufacturers, hospitals, physicians, and other sources on adverse drug reactions.Drug-Related Side Effects and Adverse Reactions: Disorders that result from the intended use of PHARMACEUTICAL PREPARATIONS. Included in this heading are a broad variety of chemically-induced adverse conditions due to toxicity, DRUG INTERACTIONS, and metabolic effects of pharmaceuticals.Pharmacovigilance: The detection of long and short term side effects of conventional and traditional medicines through research, data mining, monitoring, and evaluation of healthcare information obtained from healthcare providers and patients.Heart Rate: The number of times the HEART VENTRICLES contract per unit of time, usually per minute.Sinoatrial Node: The small mass of modified cardiac muscle fibers located at the junction of the superior vena cava (VENA CAVA, SUPERIOR) and right atrium. Contraction impulses probably start in this node, spread over the atrium (HEART ATRIUM) and are then transmitted by the atrioventricular bundle (BUNDLE OF HIS) to the ventricle (HEART VENTRICLE).Depression, Chemical: The decrease in a measurable parameter of a PHYSIOLOGICAL PROCESS, including cellular, microbial, and plant; immunological, cardiovascular, respiratory, reproductive, urinary, digestive, neural, musculoskeletal, ocular, and skin physiological processes; or METABOLIC PROCESS, including enzymatic and other pharmacological processes, by a drug or other chemical.Nizatidine: A histamine H2 receptor antagonist with low toxicity that inhibits gastric acid secretion. The drug is used for the treatment of duodenal ulcers.Granulocytes: Leukocytes with abundant granules in the cytoplasm. They are divided into three groups according to the staining properties of the granules: neutrophilic, eosinophilic, and basophilic. Mature granulocytes are the NEUTROPHILS; EOSINOPHILS; and BASOPHILS.Erythrocyte Deformability: Ability of ERYTHROCYTES to change shape as they pass through narrow spaces, such as the microvasculature.Filtration: A process of separating particulate matter from a fluid, such as air or a liquid, by passing the fluid carrier through a medium that will not pass the particulates. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)Sialorrhea: Increased salivary flow.Anesthesia, Local: A blocking of nerve conduction to a specific area by an injection of an anesthetic agent.Salivation: The discharge of saliva from the SALIVARY GLANDS that keeps the mouth tissues moist and aids in digestion.Analgesics, Opioid: Compounds with activity like OPIATE ALKALOIDS, acting at OPIOID RECEPTORS. Properties include induction of ANALGESIA or NARCOSIS.Benzodiazepines: A group of two-ring heterocyclic compounds consisting of a benzene ring fused to a diazepine ring.Hemodynamics: The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.Anti-Anxiety Agents: Agents that alleviate ANXIETY, tension, and ANXIETY DISORDERS, promote sedation, and have a calming effect without affecting clarity of consciousness or neurologic conditions. ADRENERGIC BETA-ANTAGONISTS are commonly used in the symptomatic treatment of anxiety but are not included here.Carbonic Anhydrase Inhibitors: A class of compounds that reduces the secretion of H+ ions by the proximal kidney tubule through inhibition of CARBONIC ANHYDRASES.Miotics: Agents causing contraction of the pupil of the eye. Some sources use the term miotics only for the parasympathomimetics but any drug used to induce miosis is included here.Glaucoma, Open-Angle: Glaucoma in which the angle of the anterior chamber is open and the trabecular meshwork does not encroach on the base of the iris.Acetazolamide: One of the CARBONIC ANHYDRASE INHIBITORS that is sometimes effective against absence seizures. It is sometimes useful also as an adjunct in the treatment of tonic-clonic, myoclonic, and atonic seizures, particularly in women whose seizures occur or are exacerbated at specific times in the menstrual cycle. However, its usefulness is transient often because of rapid development of tolerance. Its antiepileptic effect may be due to its inhibitory effect on brain carbonic anhydrase, which leads to an increased transneuronal chloride gradient, increased chloride current, and increased inhibition. (From Smith and Reynard, Textbook of Pharmacology, 1991, p337)Carbonic Anhydrases: A family of zinc-containing enzymes that catalyze the reversible hydration of carbon dioxide. They play an important role in the transport of CARBON DIOXIDE from the tissues to the LUNG. EC 4.2.1.1.Intraocular Pressure: The pressure of the fluids in the eye.Methazolamide: A carbonic anhydrase inhibitor that is used as a diuretic and in the treatment of glaucoma.

Neuroregulation by vasoactive intestinal peptide (VIP) of mucus secretion in ferret trachea: activation of BK(Ca) channels and inhibition of neurotransmitter release. (1/296)

1. The aims of this study were to determine: (1) whether vasoactive intestinal peptide (VIP) regulates cholinergic and 'sensory-efferent' (tachykininergic) 35SO4 labelled mucus output in ferret trachea in vitro, using a VIP antibody, (2) the class of potassium (K+) channel involved in VIP-regulation of cholinergic neural secretion using glibenclamide (an ATP-sensitive K+ (K(ATP)) channel inhibitor), iberiotoxin (a large conductance calcium activated K+ (BK(ca)) channel blocker), and apamin (a small conductance K(ca) (SK(ca)) channel blocker), and (3) the effect of VIP on cholinergic neurotransmission using [3H]-choline overflow as a marker for acetylcholine (ACh) release. 2. Exogenous VIP (1 and 10 microM) alone increased 35SO4 output by up to 53% above baseline, but suppressed (by up to 80% at 1 microM) cholinergic and tachykininergic neural secretion without altering secretion induced by ACh or substance P (1 microM each). Endogenous VIP accounted for the minor increase in non-adrenergic, non-cholinergic (NANC), non-tachykininergic neural secretion, which was compatible with the secretory response of exogenous VIP. 3. Iberiotoxin (3 microM), but not apamin (1 microM) or glibenclamide (0.1 microM), reversed the inhibition by VIP (10 nM) of cholinergic neural secretion. 4. Both endogenous VIP (by use of the VIP antibody; 1:500 dilution) and exogenous VIP (0.1 microM), the latter by 34%, inhibited ACh release from cholinergic nerve terminals and this suppression was completely reversed by iberiotoxin (0.1 microM). 5. We conclude that, in ferret trachea in vitro, endogenous VIP has dual activity whereby its small direct stimulatory action on mucus secretion is secondary to its marked regulation of cholinergic and tachykininergic neurogenic mucus secretion. Regulation is via inhibition of neurotransmitter release, consequent upon opening of BK(Ca) channels. In the context of neurogenic mucus secretion, we propose that VIP joins NO as a neurotransmitter of i-NANC nerves in ferret trachea.  (+info)

alpha-adrenergic stimulation mediates glucose uptake through phosphatidylinositol 3-kinase in rat heart. (2/296)

We examined whether insulin and catecholamines share common pathways for their stimulating effects on glucose uptake. We perfused isolated working rat hearts with Krebs-Henseleit buffer containing [2-3H]glucose (5 mmol/L, 0.05 microCi/mL) and sodium oleate (0.4 mmol/L). In the absence or presence of the phosphatidylinositol 3-kinase (PI3-K) inhibitor wortmannin (3 micromol/L), we added insulin (1 mU/mL), epinephrine (1 micromol/L), phenylephrine (100 micromol/L) plus propranolol (10 micromol/L, selective alpha-adrenergic stimulation), or isoproterenol (1 micromol/L) plus phentolamine (10 micromol/L, selective beta-adrenergic stimulation) to the perfusate. Cardiac power was found to be stable in all groups (between 8.07+/-0.68 and 10.7+/-0. 88 mW) and increased (25% to 47%) with addition of epinephrine, but not with selective alpha- and beta-adrenergic stimulation. Insulin and epinephrine, as well as selective alpha- and beta-receptor stimulation, increased glucose uptake (the following values are in micromol/[min. g dry weight]: basal, 1.19+/-0.13; insulin, 3.89+/-0.36; epinephrine, 3.46+/-0.27; alpha-stimulation, 4.08+/-0.40; and beta-stimulation, 3.72+/-0.34). Wortmannin completely inhibited insulin-stimulated and selective alpha-stimulated glucose uptake, but it did not affect the epinephrine-stimulated or selective beta-stimulated glucose uptake. Sequential addition of insulin and epinephrine or insulin and alpha-selective stimulation showed additive effects on glucose uptake in both cases. Wortmannin further blocked the effects of insulin on glycogen synthesis. We conclude that alpha-adrenergic stimulation mediates glucose uptake in rat heart through a PI3-K-dependent pathway. However, the additive effects of alpha-adrenergic stimulation and insulin suggest 2 different isoforms of PI3-K, compartmentation of PI3-K, potentiation, or inhibition by wortmannin of another intermediate of the alpha-adrenergic signaling cascade. The stimulating effects of both the alpha- and the beta-adrenergic pathways on glucose uptake are independent of changes in cardiac performance.  (+info)

S-16924, a novel, potential antipsychotic with marked serotonin1A agonist properties. IV. A drug discrimination comparison with clozapine. (3/296)

The novel benzodioxopyrrolidine (S-16924) displays a clozapine-like profile of interaction with multiple monoaminergic receptors, in addition to potent agonist activity at serotonin (5-HT)1A receptors. S-16924 (2.5 mg/kg i.p.) and clozapine (5.0 mg/kg i.p.) generated robust discriminative stimuli (DS) and displayed full mutual generalization. The D4 antagonists L-745,870 and S-18126, the D1/D5 antagonist SCH-39166, and the D3 antagonist S-14297 showed at most partial generalization to S-16924 and clozapine. The D2/D3 antagonist raclopride fully generalized to S-16924, but only partially generalized to clozapine. The 5-HT2A antagonist MDL-100, 907 fully generalized to S-16924 and two further 5-HT2A antagonists, fananserin and SR-46349, showed partial generalization. However, MDL-100,907, fananserin, and SR-46349 showed less pronounced generalization to clozapine. Similarly, the 5-HT2C antagonists SB-200,646 and SB-206,553 more markedly generalized to S-16924 than to clozapine. The 5-HT1A receptor agonist (+/-)-8-dihydroxy-2-(di-n-propylamino) tetralin generalized fully to S-16924 but not to clozapine. Full generalization was obtained to both S-16924 and clozapine for the clozapine congeners, olanzapine and quetiapine. In distinction, the benzisoxazole, risperidone, and the phenylindole, sertindole, weakly generalized to S-16924 and clozapine. However, the benzisoxazole ziprasidone, which possesses 5-HT1A agonist properties, generalized fully to S-16924 but not to clozapine. Finally, the muscarinic antagonist scopolamine generalized fully to clozapine and partially to S-16924. In conclusion, S-16924 and clozapine display both communalities and differences in their "compound" DS; this likely reflects their respective complex patterns of interaction with multiple monoaminergic receptors. Although no specific receptor was identified as underlying the clozapine DS, 5-HT1A agonist as well as D2 and 5-HT2A/2C antagonist properties contribute to the S-16924 DS.  (+info)

beta2-adrenergic cAMP signaling is uncoupled from phosphorylation of cytoplasmic proteins in canine heart. (4/296)

BACKGROUND: Recent studies of beta-adrenergic receptor (beta-AR) subtype signaling in in vitro preparations have raised doubts as to whether the cAMP/protein kinase A (PKA) signaling is activated in the same manner in response to beta2-AR versus beta1-AR stimulation. METHODS AND RESULTS: The present study compared, in the intact dog, the magnitude and characteristics of chronotropic, inotropic, and lusitropic effects of cAMP accumulation, PKA activation, and PKA-dependent phosphorylation of key effector proteins in response to beta-AR subtype stimulation. In addition, many of these parameters and L-type Ca2+ current (ICa) were also measured in single canine ventricular myocytes. The results indicate that although the cAMP/PKA-dependent phosphorylation cascade activated by beta1-AR stimulation could explain the resultant modulation of cardiac function, substantial beta2-AR-mediated chronotropic, inotropic, and lusitropic responses occurred in the absence of PKA activation and phosphorylation of nonsarcolemmal proteins, including phospholamban, troponin I, C protein, and glycogen phosphorylase kinase. However, in single canine myocytes, we found that beta2-AR-stimulated increases in both ICa and contraction were abolished by PKA inhibition. Thus, the beta2-AR-directed cAMP/PKA signaling modulates sarcolemmal L-type Ca2+ channels but does not regulate PKA-dependent phosphorylation of cytoplasmic proteins. CONCLUSIONS: These results indicate that the dissociation of beta2-AR signaling from cAMP regulatory systems is only apparent and that beta2-AR-stimulated cAMP/PKA signaling is uncoupled from phosphorylation of nonsarcolemmal regulatory proteins involved in excitation-contraction coupling.  (+info)

Neurometabolic effects of psilocybin, 3,4-methylenedioxyethylamphetamine (MDE) and d-methamphetamine in healthy volunteers. A double-blind, placebo-controlled PET study with [18F]FDG. (5/296)

The neurometabolic effects of the hallucinogen psilocybin (PSI; 0.2 mg/kg), the entactogen 3,4-methylenedioxyethylamphetamine (MDE; 2 mg/kg) and the stimulant d-methamphetamine (METH; 0.2-0.4 mg/kg) and the drugs' interactions with a prefrontal activation task were investigated in a double-blind, placebo-controlled human [F-18]fluorodeoxyglucoseFDG-positron emission tomographicPET study (each group: n = 8). Subjects underwent two scans (control: word repetition; activation word association) within 2-4 weeks. Psilocybin increased rMRGlu in distinct right hemispheric frontotemporal cortical regions, particularly in the anterior cingulate and decreased rMRGlu in the thalamus. Both MDE and METH induced cortical hypometabolism and cerebellar hypermetabolism. In the MDE group, cortical hypometabolism was more pronounced in frontal regions, with the exception of the right anterior cingulate, which tended to be hyperactive. Cognitive activation-related increases in left frontocortical regions were attenuated under all three psychoactive substances, but less so under MDE. Taking into account performance data and subjective reports on task difficulty, these effects may result from different mechanisms across the three groups. Our PSI data are in line with studies on acute schizophrenic patients suggesting frontal overactivity at rest, but diminished capacity to activate prefrontal regions upon cognitive demand. The MDE data support the hypothesis that entactogens constitute a distinct psychoactive substance class, which takes an intermediate position between stimulants and hallucinogens.  (+info)

Glucose uptake during centrally induced stress is insulin independent and enhanced by adrenergic blockade. (6/296)

Glucose utilization increases markedly in the normal dog during stress induced by the intracerebroventricular (ICV) injection of carbachol. To determine the extent to which insulin, glucagon, and selective (alpha/beta)-adrenergic activation mediate the increment in glucose metabolic clearance rate (MCR) and glucose production (R(a)), we used five groups of normal mongrel dogs: 1) pancreatic clamp (PC; n = 7) with peripheral somatostatin (0.8 microg x kg(-1) x min(-1)) and intraportal replacement of insulin (1,482 +/- 84 pmol x kg(-1) x min(-1)) and glucagon (0.65 ng x kg(-1) x min(-1)) infusions; 2) PC plus combined alpha (phentolamine)- and beta (propranolol)-blockade (7 and 5 microg x kg(-1) x min(-1), respectively; alpha+beta; n = 5); 3) PC plus alpha-blockade (alpha; n = 6); 4) PC plus beta-blockade (beta; n = 5); and 5) a carbachol control group without PC (Con; n = 10). During ICV carbachol stress (0-120 min), catecholamines, ACTH, and cortisol increased in all groups. Baseline insulin and glucagon levels were maintained in all groups except Con, where glucagon rose 33%, and alpha, where insulin increased slightly but significantly. Stress increased (P < 0.05) plasma glucose in Con, PC, and alpha but decreased it in beta and alpha+beta. The MCR increment was greater (P < 0.05) in beta and alpha+beta than in Con, PC, and alpha. R(a) increased (P < 0.05) in all groups but was attenuated in alpha+beta. Stress-induced lipolysis was abolished in beta (P < 0.05). The marked rise in lactate in Con, PC, and alpha was abolished in alpha+beta and beta. We conclude that the stress-induced increase in MCR is largely independent of changes in insulin, markedly augmented by beta-blockade, and related, at least in part, to inhibition of lipolysis and glycogenolysis, and that R(a) is augmented by glucagon and alpha- and beta-catecholamine effects.  (+info)

beta-adrenergic agonists stimulate Na+-K+-Cl- cotransport by inducing intracellular Ca2+ liberation in crypt cells. (7/296)

Epinephrine and beta-adrenergic agonists (beta1 and beta2 for isoproterenol, beta1 for dobutamine, beta2 for salbutamol) stimulated K+ (or 86Rb) influx mediated by the Na+-K+-2Cl- cotransporter and the Na+-K+ pump in isolated colonic crypt cells. Preincubation with bumetanide abolished the epinephrine effect on the Na+-K+ pump, suggesting that the primary effect is on the cotransporter. Maximal effect was obtained with 1 microM epinephrine with an EC50 of 91.6 +/- 9.98 nM. Epinephrine-induced K+ transport was blocked by propranolol with an IC50 of 134 +/- 28.2 nM. alpha-Adrenergic drugs did not modify K+ transport mechanisms. Neither Ba2+ nor tetraethylammonium nor DIDS modified the adrenergic enhancement on the cotransporter. In addition, epinephrine did not affect K+ efflux. Dibutyryl cAMP did not alter K+ transport. Reduction of extracellular Ca2+ to 30 nM did not influence the response to epinephrine. However, 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-AM abolished epinephrine-induced K+ transport. Ionomycin increased Na+-K+-2Cl- cotransport activity. Moreover, epinephrine increased intracellular Ca2+ concentration in a process inhibited by propranolol. In conclusion, epinephrine stimulated the Na+-K+-2Cl- cotransporter in a process mediated by beta1- and beta2-receptors and modulated by intracellular Ca2+ liberation.  (+info)

Sympathetic inhibition, leptin, and uncoupling protein subtype expression in normal fasting rats. (8/296)

To further investigate neural effects on leptin and uncoupling proteins (UCPs), we studied in vivo perturbations intended to block adrenergic input to peripheral tissues. We examined plasma leptin, leptin mRNA, and adipose and muscle UCP subtype mRNA in rats treated with alpha-methyl-p-tyrosine methyl ester (AMPT-ME), which inhibits catecholamine synthesis and 6-hydroxydopamine (6HDA), which is toxic to catecholinergic nerve terminals but, unlike AMPT-ME, does not enter the central nervous system. Intraperitoneal AMPT-ME, 250 mg/kg, was administered at 1800 and 0700 the following day, and rats were killed at 1200-1400. All rats were fasted with free access to water during this time. Intraperitoneal AMPT-ME increased plasma leptin by 15-fold, increased interscapular brown adipose tissue (IBAT) and epididymal fat leptin mRNA by 2- to 2.5-fold, and also increased plasma insulin and glucose concentrations. Intraperitoneal AMPT-ME decreased IBAT UCP-3 mRNA to 40% of control, while it increased epididymal adipose UCP-3 mRNA approximately twofold. Intravenous AMPT-ME, 250 mg/kg, administered to conscious rats for 5 h decreased lumbar sympathetic nerve activity, increased plasma leptin (5.89 +/- 1.43 compared with 2.75 +/- 0.31 ng/ml in vehicle-treated rats, n = 7, P < 0.05), and decreased cardiac rate with no sustained change in blood pressure. Intraperitoneal 6HDA, 100 mg/kg, as a single dose at 1800, increased plasma leptin approximately twofold after 18-20 h, increased IBAT (but not epididymal fat) leptin mRNA by two- to threefold, and decreased IBAT UCP-3 mRNA to 30-40% of control. Neither AMPT-ME nor 6HDA significantly altered mRNA encoding gastrocnemius muscle UCP-3, IBAT UCP-1, or IBAT and epididymal UCP-2. In summary, AMPT-ME and 6HDA increased plasma leptin and upregulated leptin mRNA expression. AMPT-ME also resulted in complex tissue and subtype-specific modulation of adipose UCP mRNA. These data are consistent with interaction between leptin and sympathetic nerve activity (SNA) in regulation of fat cell energy utilization. However, the in vivo modulation of leptin and UCPs appears complex and, beyond a causal effect of SNA per se, may depend on concurrent changes in plasma insulin, glucose, and circulatory hemodynamics.  (+info)

Commissioner Weston asked if we are going to try to make this policy cover those types of projects like we ran into in Cache Valley with the sidewalk program. Howard Richardson replied that the policy principally deals with curb, gutter and sidewalk replacement; the management, jurisdiction and maintenance of it. Commissioner Weston referred to a section of the policy which says, ". . . on Federal-aid projects where the facilities are not eligible for Federal funds any funds made available by legislative appropriations, contributions of property owners, cities, counties, other parties or any combination of the foregoing will be used." He said that seems pretty inclusive and covers most any sidewalk with which were involved whether its sidewalk money, or any other kind. His concern, as he has mentioned before, is that we pass the money through in the sidewalk program, and then let it die. They put the sidewalks in and we may look at them or we may not. Are we looking at that closely enough when ...
The effect of beta adrenergic agents on granulocyte deformability was investigated using the filtration technique. Three groups of granulocytes were studied: 1) cells treated with isoproterenol (10−6 to 10−3 M); 2) cells treated with propranolol (10−
Atenololo, un beta competitivo (1)-adrenergici antagonista selettivo, ha la più bassa solubilità lipidica di questa classe di farmaci. Anche se è simile al metoprololo, atenololo differisce da pindololo e propranololo in quanto non ha caratteristiche intrinseche simpaticomimetica o attività stabilizzante di membrana. Latenololo è usato da solo o con clortalidone nella gestione di ipertensione ed edema ...
The role of norepinephrine in the development of amygdaloid kindling in rats was investigated. In the first experiment, pretreatment with the noradrenergic neurotoxin, DSP-4 (63 mg/kg, ip), whose action is reportedly specific to locus coeruleus neurons, markedly accelerated the rate of kindling. DSP-4 treated animals and saline controls required 3.8 and 7.5 after-discharges (ADs) to kindle respectively. Furthermore, DSP-4 treatment lengthened the latency of the onset to clonus during the first stage 5 seizure. Norepinephrine levels measured in the telencephalon were lowered by 45% with DSP-4 treatment, whereas dopamine and 5-hydroxytryptamine levels were unaffected. -- In an attempt to test the hypothesis that a tonic presence of norepinephrine serves to inhibit kindling development, rats were treated with DSP-4, and chronically infused (icv) with either norepinephrine (5 ug/.5 ul/hr), or the vehicle, via an osmotic minipump. Telencephalic norepinephrine levels were not raised by the infusion of ...
Heuer, A., Smith, G. A. and Dunnett, S. B. (2013), Comparison of 6-hydroxydopamine lesions of the substantia nigra and the medial forebrain bundle on a lateralised choice reaction time task in mice. European Journal of Neuroscience, 37: 294-302. doi: 10.1111/ejn.12036 ...
Buy High Quality Double Sided PET Tape DSP-150GH, Find Details include Size,Weight,Model and Width about High Quality Double Sided PET Tape DSP-150GH. Make an Inquiry for High Quality Double Sided PET Tape DSP-150GH at OKorder.com.
RT-PCR data showed that the mRNA levels of gammaGCS, the rate-limiting enzyme of gamma-L-glutamyl-L-cysteinylglycine (GSH) synthesis, were increased by 6-OHDA after treatment for 24 h and 48 h; the mRNA levels of GPx, GR, and GST did not alter in 6-OHDA-treated astrocytes after treatment for 24 h and 48 h; and 6-OHDA increased the mRNA levels and the activity of gammaGT after treatment for 48 h, which induced a decrease in GSx levels, despite the up-regulation of gammaGCS after exposure to 6-OHDA for 48 h." (15960885) ...
The adrenergic amines noradrenaline and adrenaline increased flux through phenylalanine hydroxylase by approx. 50%. This effect, which appears to be mediated by an alpha-adrenergic mechanism, was accompanied by a rapid increase in the phosphorylation of phenylalanine hydroxylase. Although ionophore A23187 mimicked the effects of the adrenergic amines, vasopressin was completely without effect on either phenylalanine hydroxylation or enzyme phosphorylation. Flux through phenylalanine hydroxylase in young rats (80 g) was insensitive to alpha-adrenergic, but sensitive to beta-adrenergic, agents. Consistent with previous observations [Fisher & Pogson (1984) Biochem. J. 219, 79-85] the present data indicate a close correlation between phosphorylation state and flux rate (i.e. enzyme activity). ...
The lack of β-adrenergic modulation in VEDS cardiomyocytes suggests that one or more components of the signaling cascade were missing or functionally inactive. To identify these components, we assayed the functional activity of different elements in the β-adrenergic enzymatic cascade. A key finding was that ICaL was strongly stimulated by cell dialysis with the catalytic subunit of PKA in both VEDS and LDS cardiomyocytes. In contrast to a previous report6 in which fast current rundown was observed using Ba2+ as a charge carrier, we could accurately measure the stimulating effect of the catalytic subunit of PKA on ICaL in VEDS cardiomyocytes. The catalytic subunit of PKA produced a maximal ICaL stimulation. Importantly, ICaL stimulation by the catalytic subunit of PKA was found to be similar (≈3 times) in VEDS, LDS, and ventricular cardiomyocytes isolated from the adult mouse heart. These data provide strong evidence for similar structural properties of the Ca2+ channel or a closely related ...
Anfetamine e destroanfetamina, agenti sypathomimetic non catechloamine, sono utilizzati in combinazione per il trattamento di deficit di attenzione e iperattività (ADHD) o di narcolessia. Adderall è costituito da equivalente quantità di aspartato anfetamine, solfato di anfetamina, saccarato destroanfetamina e solfato destroanfetamina ...
|p|This high a quality ELISA from Randox Food is available for the detection of zilpaterol present in fish, shrimp and other seafood tissue.|/p|
OBJECTIVE: Myocardial damage induced by isoproterenol is believed to be secondary to increased oxygen demands on the heart. Our objective was to test an additional primary action of isoproterenol on tissue and mitochondrial oxidative metabolism and to compare these effects with the effects of other adrenergic agents in the presence of adrenergic inhibitors. DESIGN: Prospective, dose-response study. SETTING: Research laboratory at a university hospital. SUBJECTS: Fifty Sprague-Dawley female rats (200 to 350 g), slightly anesthetized with ether and divided into several groups. INTERVENTIONS: In 26 rats, the heart was removed, cut into fine slices (0.5-mm thickness), and placed in an ice-cold buffer. In 22 animals, the hearts were perfused in the Langendorff manner and chopped and processed for mitochondrial studies. MEASUREMENTS AND MAIN RESULTS: We determined the following: a) the direct "in vitro" effects of isoproterenol and related catecholamines on normal oxygen uptake using myocardial ...
3H]Dihydroergocryptine, a nonselective alpha adrenergic antagonist, the alpha-1 selective antagonist, [3H]prazosin and the alpha-2 selective antagonist, [3H]yohimbine, were used to study binding sites in rat renal membranes. To establish a correlation between binding and a biological function, the ability of alpha adrenergic agents to stimulate or inhibit vasoconstriction was quantified in vitro using an isolated perfused kidney preparation. Binding with each radioligand was rapid, saturable and specific. Moreover, the order of potencies of a variety of adrenergic agents, determined by competitive inhibition studies, suggested that the binding of each radioligand was to sites with alpha adrenergic specificity. The total number of binding sites in these rat renal membranes. determined with [3H]dihydroergocryptine (Bmax, 212 fmol/mg of protein; KD, 12.8 nM) was approximately equal to the sum of binding site concentrations determined with the alpha-1 and alpha-2 selective radioligands (Bmax, 57 and ...
&splt;p>Sagger Mawri, MD and Khalid George, MD&splt;/p> &splt;p>December 11, 2015&splt;/p> &splt;p>A 64-year-old woman with history of lumbar compression fracture status post L3-L5 kyphoplasty two weeks prior presented to the emergency department complaining of worsening lower extremity weakness since her spinal surgery. Her symptoms became severe and limited her ability to stand or ambulate. She also endorsed urinary and bowel incontinence. On examination, she demonstrated moderately reduced bilateral lower extremity strength and reduced rectal tone without sensory deficits or clonus. Computed tomography with contrast is obtained.&spamp;nbsp;&splt;/p> &splt;div>&splt;img src=&doublequot;http://www.sgim.org/Image Library/JGIM/Web Only/Clinical Images/Cement-in-IVC.jpg&doublequot; alt=&doublequot;cement in ivc&doublequot; objectid=&doublequot;2e147345-cd18-4229-b9dd-0c7bcc216c14&doublequot; imagesiteid=&doublequot;8039ce09-e7da-47e1-bcec-df96b5e411f4&doublequot; />&splt;/div> &splt;p>&spamp;nbsp;&splt;/p
In the present study, in agreement with others (Breese and Traylor, 1971, 1972; Breese et al., 1984), there was an extensive reduction in the neostriatal content of DA (97%), HVA (98%) and DOPAC (89%) in 6-OHDA-treated rats, regardless of HAL treatment (table 1). Neostriatal NE content was unaltered, probably reflecting effectiveness of desipramine pretreatment in protecting noradrenergic neurons from 6-OHDA destruction. As expected, neostriatal concentrations of 5-HT and 5-HIAA were significantly elevated by neonatal 6-OHDA treatment (table 1, P , .01), reflecting the known proliferative sprouting of 5-HT fibers in the forebrain of rats lesioned neonatally with 6-OHDA (Stachowiak et al., 1984;Berger et al., 1985; Snyder et al., 1986).. Spontaneous oral activity of intact rats remained at a consistently low level for the entire duration of the experiment (fig. 1). Also, neonatal 6-OHDA treatment alone did not increase the level of spontaneous oral activity (fig. 1). The HAL dose (1.5 mg/kg/day) ...
Guanethidine Sulfate is a medicine available in a number of countries worldwide. A list of US medications equivalent to Guanethidine Sulfate is available on the Drugs.com website.
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Close The Infona portal uses cookies, i.e. strings of text saved by a browser on the users device. The portal can access those files and use them to remember the users data, such as their chosen settings (screen view, interface language, etc.), or their login data. By using the Infona portal the user accepts automatic saving and using this information for portal operation purposes. More information on the subject can be found in the Privacy Policy and Terms of Service. By closing this window the user confirms that they have read the information on cookie usage, and they accept the privacy policy and the way cookies are used by the portal. You can change the cookie settings in your browser. ...
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光大 guāngdà, splendid/magnificent/abbr. for 中國光大銀行,中国光大银行[Zhōng guó Guāng dà Yín háng], China ...
Adrenergic blocking agents. V. 1-Amino-3-(substituted phenoxy)-2-propanols". Journal of Medicinal Chemistry. 12 (4): 638. doi: ... Prenalterol interestingly exhibits adrenergic agonist activity in spite of an interposed oxymethylene group. The stereospecific ... with isopropylamine followed by hydrogenolytic removal of the O-benzyl ether affords the β1-adrenergic selective adrenergic ...
alpha-2 adrenergic agentsEdit. Rebound hypertension, above pre-treatment level, was observed after clonidine,[15] and ...
Walker, Susannah B.; Kradjan, Wayne A.; Bierman, C. Warren (6 May 1985). "Bitolterol Mesylate: A Beta-adrenergic Agent; ... Bitolterol mesylate (Tornalate) is a short-acting β2 adrenergic receptor agonist used for the relief of bronchospasm in ...
1977), "Adrenergic agents. 4. Substituted phenoxypropanolamine derivatives as potential β-adrenergic agonists" (in German), J. ... 1978), "Nondepressant β-adrenergic blocking agents. 1. Substituted 3-amino-1-(5,6,7,8-tetrahydro-1-naphthoxy)-2-propanols" (in ... It is used as starting material for agricultural and pharmaceutical agents. The carbon skeleton of 1-tetralone is also found in ...
A Beta-adrenergic Agent; Chemistry, Pharmacokinetics, Pharmacodynamics, Adverse Effects and Clinical Efficacy in Asthma". ...
Gross ME (2001). "Tranquilizers, α2-adrenergic agonists, and related agents". In Adams RH. Veterinary Pharmacology and ... A reversal agent for benzodiazepines exists, flumazenil (Anexate). Its use as an antidote is not routinely recommended because ... Although they are second-line agents, benzodiazepines can be used for a limited time to relieve severe anxiety and agitation. ... Kintz P (2007). "Bioanalytical procedures for detection of chemical agents in hair in the case of drug-facilitated crimes". ...
... is an antihypertensive agent. It is used in the form of its sulfate. Guanadrel is a postganglionic adrenergic ... blocking agent. Uptake of guanadrel and storage in sympathetic neurons occurs via the norepinephrine pump; guanadrel slowly ...
Direct intraspinal injection of the catecholamines epinephrine and norepinephrine, and the α-adrenergic agents dexmedetomidine ... "Spinal administration of adrenergic agents produces analgesia in amphibians". European Journal of Pharmacology. 316 (2): 205- ... The relative analgesic potency of 11 opioid agents (μ-opioid receptor agonists - fentanyl, levorphanol, methadone, morphine, ... relative analgesic potency of μ-opioids in amphibians was correlated with the relative analgesic potency of these same agents ...
Kjaergaard N, Kjaergaard B, Lauritsen JG (June 1988). "Prazosin, an adrenergic blocking agent inadequate as male contraceptive ... It is also used in complex regional pain syndrome (CRPS) type 1 due to its anti-adrenergic affects. It has shown to be ... Phenoxybenzamine forms a permanent covalent bond with adrenergic receptors. Based on known information about the structures of ... "Phenoxybenzamine binding reveals the helical orientation of the third transmembrane domain of adrenergic receptors". J. Biol. ...
It is a sympathomimetic agent with marked alpha adrenergic activity. It is a vasoconstrictor with a rapid action in reducing ...
Tafreshi MJ, Weinacker AB (August 1999). "Beta-adrenergic-blocking agents in bronchospastic diseases: a therapeutic dilemma". ... Bakris G (May 2009). "An in-depth analysis of vasodilation in the management of hypertension: focus on adrenergic blockade". J ... For this reason, beta blockers that selectively block β1 adrenergic receptors (termed cardioselective or β1-selective beta ... Galougahi, Keyvan (February 19, 2016). "β3 Adrenergic Stimulation Restores Nitric Oxide/Redox Balance and Enhances Endothelial ...
Kjaergaard N, Kjaergaard B, Lauritsen JG; Kjaergaard; Lauritsen (June 1988). "Prazosin, an adrenergic blocking agent inadequate ...
Falkay, G.; Kovács, L. (1986). "Affinity of tocolytic agents on human placental and myometrial beta-adrenergic receptors". ... Giorgino, F. L.; Egan, C. G. (2010). "Use of isoxsuprine hydrochloride as a tocolytic agent in the treatment of preterm labour ...
Sympatholytic agents, such as the alpha-adrenergic blocker prazosin, may provide temporary relief. Losartan can, and topical ...
"Cardiovascular Adverse Drug Reaction Associated with Combined β-Adrenergic and Calcium Entry-Blocking Agents". Journal of ... Peroutka, Stephen J. (1983). "The Pharmacology of Calcium Channel Antagonists: a Novel Class of Anti-migraine Agents?". ...
"Characterization of the Adrenergic Activity of Arbutamine, a Novel Agent for Pharmacological Stress Testing". Cardiovascular ... It stimulates β adrenergic receptors. Abou-Mohamed, Gamal; Nagarajan, Ravi; Ibrahim, Tarek M.; Caldwell, Robert W. (March 1996 ...
These agents also commonly have action at α-adrenergic receptors and/or 5-HT receptors. This lack of receptor selectivity is ... Agents where the main therapeutic effect is mediated by negative modulation of histamine receptors are termed antihistamines; ... They can be classified on the basis of chemical structure, and agents within these groups have similar properties. Two aromatic ... Patient response and occurrence of adverse drug reactions vary greatly between classes and between agents within classes. The ...
... (AY-28,228) is an antihypertensive agent which acts as a selective α1-adrenergic receptor antagonist. It also ... A new class of potent antihypertensive agents". Journal of Medicinal Chemistry. 30 (2): 388-94. doi:10.1021/jm00385a022. PMID ... Prazosin Ketanserin David J. Triggle (1996). Dictionary of Pharmacological Agents. Boca Raton: Chapman & Hall/CRC. ISBN 0-412- ...
... can also be a side effect of alpha-1 blockers (alpha1 adrenergic blocking agents). Alpha1 blockers ...
for pioneering signal transduction therapy and for developing tyrosine kinase inhibitors as effective agents against cancer and ... for developing agents which block beta adrenergic and histamine receptors.. 1983/4 Не присуждалась ...
... is an antiarrhythmic agent, chemically related in structure to beta-adrenergic receptor blocker drugs such as ... Warembourg H, Ducloux G. [Clinical study of a new anti-arrhythmia agent: nadoxolol]. Lille Med. 1976;21(4 Suppl 2):386-8. PMID ... an intermediate in the synthesis of beta-adrenergic receptor blockers". Bioorganic Chemistry. 31 (3): 259-69. PMID 12818235. ...
Other stimulators include the powerful vasoconstriction-inducing agents, angiotensin II, endothelins, and alpha adrenergic ... Many agents stimulate cells and tissues to produce 20-HETE in vitro and in vivo. Androgens are particularly potent stimulators ... There are a variety of pharmacological agents which inhibit the synthesis of 20-HETE including various fatty acid analogs that ... Drugs that are substrates for the UGT enzymes which metabolize 20-HETE such as non-steroidal anti-inflammatory agents, opioids ...
Imidazolines are sympathomimetic agents, with primary effects on α adrenergic receptors and little if any effect on β ... Oxymetazoline is a selective α1 adrenergic receptor agonist and α2 adrenergic receptor partial agonist. It is a topical ... α2 adrenergic receptors. Since vascular beds widely express α1 receptors, the action of oxymetazoline results in ... although its pharmacological effects may be reversed by α adrenergic antagonists such as phentolamine. In the event of a ...
"In vivo and in vitro Characterization of the Novel Antiarrhythmic Agent SSR149744C: Electrophysiological, Anti-adrenergic, and ... Celivarone has potential as an antiarrhythmic agent, attributable to its multifactorial mechanism of action; blocking Na+, L- ... Arrhythmias can also be induced by altered activity of the vagus nerve and activation of β1 adrenergic receptors. Celivarone is ...
However, there is little, if any, empirical evidence that vasoactive drugs (α-adrenergic blocking agents or calcium channel ...
... increase beta adrenergic receptors while decreasing alpha adrenergic receptors- which results in increased levels of ... Prostate cancer may be treated by removing the major source of testosterone: testicle removal (orchiectomy); or agents which ...
adrenergic blocking agent synonyms, adrenergic blocking agent pronunciation, adrenergic blocking agent translation, English ... dictionary definition of adrenergic blocking agent. adj. 1. Activated by or capable of releasing epinephrine or a similar ... substance, especially in the sympathetic nervous system: adrenergic receptors. ... adrenergic. (redirected from adrenergic blocking agent). Also found in: Thesaurus, Medical, Legal, Financial, Encyclopedia. ...
Adrenergic neuronal blocking agent definition at Dictionary.com, a free online dictionary with pronunciation, synonyms and ... A drug that blocks sympathetic nerve impulses but does not inhibit the responses of adrenergic receptors to epinephrine and ...
adrenergic neuron-blocking agent synonyms, adrenergic neuron-blocking agent pronunciation, adrenergic neuron-blocking agent ... 2. One empowered to act for or represent another: an authors agent; an insurance agent. 3. ... English dictionary definition of adrenergic neuron-blocking agent. n. 1. One that acts or has the power or authority to act. ... agent. → وَكِيل agent agent Vertreter πράκτορας agente agentti agent agent agente 代理人 대리인 agent agent agent agente агент ombud ...
Beta2-adrenergic Agonist Agent. Class Summary. Beta-agonists relax bronchial smooth muscle by action on beta2 -receptors, with ... Sympathomimetic agents. Class Summary. Epinephrine, administered intramuscularly, is the drug of choice for the treatment of ... These agents are more effective in preventing histamine response than in reversing it. They act by competitive inhibition of ... These agents are used to treat minor allergic reactions and anaphylaxis. They prevent histamine response in sensory nerve ...
Nonetheless, acute treatment with the anticholinergic agent atropine and/or the adrenergic agonist isoproterenol may be ... Anticholinergic Agents. Class Summary. Atropine, by vagolytic effect, increases the heart rate. Although it may also be used ... Beta1/Beta2 Adrenergic Agonists. Class Summary. When given systemically, isoproterenol stimulates beta receptors in the heart, ... Isoproterenol has sympathomimetic effects; specifically, beta1- and beta2-adrenergic receptor agonist activity. ...
Beta-Adrenergic Blocking Agents. Class Summary. Beta-blockers may decrease outflow obstruction and increase ventricular ... Although propranolol is generally a short-acting agent, long-acting preparations are available. A stable liquid preparation is ... Amiodarone is categorized as a class III antiarrhythmic agent but has antiarrhythmic effects that overlap all 4 Vaughn-Williams ... Amiodarone is a complex and potent antiarrhythmic agent with multiple effects on cardiac action potential, exceedingly complex ...
Beta-blockers belong to a larger class of medicines called adrenergic inhibitors. They may be used in pills by themselves or in ...
"Adrenergic Agents" by people in Harvard Catalyst Profiles by year, and whether "Adrenergic Agents" was a major or minor topic ... Drugs that act on adrenergic receptors or affect the life cycle of adrenergic transmitters. Included here are adrenergic ... "Adrenergic Agents" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical Subject ... Gaspari R. Reply to: In a subset of PEA patients, do continuous infusions of adrenergic agents improve chances of ROSC? ...
Naltrexone and Adrenergic Agents to Reduce Heroin Use in Heroin Addicts. The safety and scientific validity of this study is ... Naltrexone and Adrenergic Agents to Reduce Heroin Use in Heroin Addicts. Official Title ICMJE Heroin Addiction Treatment: ... Naltrexone and Adrenergic Agents. Brief Summary Naltrexone is a medication that is currently used to treat drug and alcohol ...
What is adrenergic blocking agents? Meaning of adrenergic blocking agents medical term. What does adrenergic blocking agents ... Looking for online definition of adrenergic blocking agents in the Medical Dictionary? adrenergic blocking agents explanation ... Adrenergic blocking agents , definition of adrenergic blocking agents by Medical dictionary https://medical-dictionary. ... redirected from adrenergic blocking agents). Also found in: Dictionary. sympatholytic drugs Drugs that inhibit nerve impulses ...
1. alpha-adrenergic blocking agent (n.). any of various drugs that block alpha-adrenergic receptors; used in treating benign ... 2. beta-adrenergic blocking agent (n.). any of various drugs used in treating hypertension or arrhythmia; decreases force and ... rate of heart contractions by blocking beta-adrenergic receptors of the autonomic nervous system ...
What is alpha-adrenergic blocking agent? Meaning of alpha-adrenergic blocking agent medical term. What does alpha-adrenergic ... Looking for online definition of alpha-adrenergic blocking agent in the Medical Dictionary? alpha-adrenergic blocking agent ... alpha-adrenergic blocking agent (alpha-blocker) (alpha-blocking agent) any of a group of drugs that selectively inhibit the ... As with beta-adrenergic blocking agents, alpha-blocking agents compete with the catecholamines at peripheral autonomic receptor ...
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Antithyroid agents. Class Summary. Thioamides function as antithyroid agents mainly by inhibiting iodide organification and ... Now primarily used as a backup agent when other first-line agents are contraindicated because of hypersensitivity or toxicity. ... Oral contrast agents ipodate or iopanoic acid also shown to be potent inhibitors of T4-to-T3 conversion, making them ideal for ... Beta-adrenergic blocker. Class Summary. Both cardioselective and noncardioselective types are important adjuncts in treating ...
Beta 2 adrenergic receptor · Beta 2 adrenergic receptor blocking agent · Beta 2 adrenergic receptor stimulating agent · ... beta 2 adrenergic receptor · beta 2 adrenergic receptor blocking agent · beta 2 adrenergic receptor stimulating agent · ... beta 1 adrenergic receptor blocking agent · beta 2 adrenergic receptor blocking agent · beta 2 adrenergic receptor stimulating ... beta 2 adrenergic receptor · beta 2 adrenergic receptor blocking agent · beta 2 adrenergic receptor stimulating agent · ...
However, because both agents exert a negative chronotropic effect, their combined ... 0/Adrenergic beta-Antagonists; 0/Calcium Channel Blockers From MEDLINE®/PubMed®, a database of the U.S. National Library of ... Adrenergic beta-Antagonists / adverse effects*, therapeutic use. Adult. Aged. Aged, 80 and over. Bradycardia / chemically ... However, because both agents exert a negative chronotropic effect, their combined use may cause bradyarrhythmias with resultant ...
Alpha2-Adrenergic Agonists. Class Summary. Presynaptic alpha2 -adrenergic agents stimulate alpha2 adrenoreceptors in the ... Antiparkinson Agents, Dopamine Agonists. Class Summary. Dopamine agonists may improve sensory symptoms associated with RLS. ... This agent is FDA-approved for neuropathic pain associated with diabetic peripheral neuropathy or postherpetic neuralgia and as ... Agents such as pramipexole, ropinirole, and bromocriptine are less likely to produce augmentation or rebound than the ...
The effect of beta adrenergic agents on granulocyte deformability was investigated using the filtration technique. Three groups ... Effect of beta adrenergic agents on granulocyte deformability Article type: Research Article ... Abstract: The effect of beta adrenergic agents on granulocyte deformability was investigated using the filtration technique. ...
The disclosure provides cosmetic and therapeutic compositions of alpha-adrenergic agents. Compositions of the disclosure may be ... Compositions and uses of alpha-adrenergic agents - Google Patents. Compositions and uses of alpha-adrenergic agents Download ... 239000000464 Adrenergic Agents Substances 0.000 title abstract description 28 * 210000000744 Eyelids Anatomy 0.000 claims ... adrenergic agent. composition. subject. Prior art date. 2016-01-26. Legal status (The legal status is an assumption and is not ...
Alpha/Beta Adrenergic Agonists. Class Summary. These agents may be used to treat nasal congestion. ... Prokinetic Agents. Class Summary. Prokinetics are promotility agents, proposed for use with severe constipation-predominant ... Anticholinergic agents can inhibit salivation and excessive secretions of the respiratory tract before surgery. These agents ... This agent competitively inhibits histamine at the H2 receptor of the gastric parietal cells, resulting in reduced gastric acid ...
Beta-adrenergic blocking agents affect blood pressure via multiple mechanisms. Actions include negative chronotropic effect ... Antiplatelet Agents. Class Summary. Antiplatelet agents have a strong mortality benefit. There is an increased risk of bleeding ... Antithrombotic Agents. Class Summary. Antithrombotic agents, which include heparin, bivalirudin, and enoxaparin, prevent the ... Beta-adrenergic blockers. Class Summary. This category of drugs has the potential to suppress ventricular ectopy due to ...
Adrenergic agonists. Class Summary. Topical agents (sympathomimetics) decrease aqueous production and reduce resistance to ... Nonselective beta-adrenergic blocking agent that lowers IOP by reducing aqueous humor production. ... Miotic Agents. Class Summary. Contract the ciliary muscle, tightening the trabecular meshwork and allowing increased outflow of ... Topical beta-adrenergic receptor antagonists decrease aqueous humor production by the ciliary body. Adverse effects are due to ...
Acute and Chronic Effects of an Adrenergic Beta-Receptor Blocking Agent (Propranolol) in Treatment of Cardiac Arrhythmias. ... Acute and Chronic Effects of an Adrenergic Beta-Receptor Blocking Agent (Propranolol) in Treatment of Cardiac Arrhythmias ... The effects of intravenous and oral administration of propranolol, an adrenergic beta-receptor blocking agent, have been ... Acute and Chronic Effects of an Adrenergic Beta-Receptor Blocking Agent (Propranolol) in Treatment of Cardiac Arrhythmias ...
The agents duties include the... Explanation of adrenergic neuron blocking agent ... Find out information about adrenergic neuron blocking agent. a person representing a business concern, esp a travelling ... Agents are also called "intelligent agents," "personal agents" and "bots." See mobile agent, bot and workflow.. ... redirected from adrenergic neuron blocking agent). Also found in: Dictionary, Thesaurus, Medical, Legal, Financial. agent. a ...
Anti-Hypertensive Adrenergic-Blocking Agents: Effects on Sodium Balance, the Renin-Angiotensin System and Haemodynamics. M. E. ... Anti-Hypertensive Adrenergic-Blocking Agents: Effects on Sodium Balance, the Renin-Angiotensin System and Haemodynamics ... Anti-Hypertensive Adrenergic-Blocking Agents: Effects on Sodium Balance, the Renin-Angiotensin System and Haemodynamics ... Anti-Hypertensive Adrenergic-Blocking Agents: Effects on Sodium Balance, the Renin-Angiotensin System and Haemodynamics ...
  • Beta-blockers belong to a larger class of medicines called adrenergic inhibitors. (howstuffworks.com)
  • Drugs that are substrates for the UGT enzymes which metabolize 20-HETE such as non-steroidal anti-inflammatory agents, opioids, gemfibrozil, Lasix, propanol, and various COX-2 inhibitors may act as perhaps unwanted side effects to increase the levels of 20-HETE. (wikipedia.org)
  • Opioidergics also comprise allosteric modulators and enzyme affecting agents like enkephalinase inhibitors. (wikipedia.org)
  • When concomitantly administered: Beta blockers reduce or neutralize therapeutic effects of hexoprenaline Methylxanthines (caffeine, theobromine, theophylline) increase its action General anaesthetics (e.g., halothane) and adrenergic receptor agonists may increase the risk of cardiovascular side effects, such as arrhythmia Hexoprenaline is contraindicated for use with monoamine oxidase inhibitors (MAOIs), tricyclic antidepressant (TCAs), ergot alkaloids, and dihydrotachysterol. (wikipedia.org)
  • Amiodarone is a complex and potent antiarrhythmic agent with multiple effects on cardiac action potential, exceedingly complex pharmacokinetics, and extracardiac pharmacodynamics. (medscape.com)
  • beta2-AR-stimulating agents may represent important immunomodulators of the cardiac myosin-induced autoimmune process and have potential as a new therapy for myocarditis. (eurekamag.com)
  • In this study, we characterized the interactions of arbutamine, a novel catecholamine developed for use as a cardiac stress testing agent, with different adrenergic receptor subtypes in vitro. (elsevier.com)
  • Because of these actions on the cardiac action potential, it is also considered a class III antiarrhythmic agent. (pharmacycode.com)
  • Dopexamine is used in hospitals as an inotropic agent to reduce exacerbations of heart failure and to treat heart failure following cardiac surgery. (wikipedia.org)
  • Antiarrhythmic agents, also known as cardiac dysrhythmia medications, are a group of pharmaceuticals that are used to suppress abnormal rhythms of the heart (cardiac arrhythmias), such as atrial fibrillation, atrial flutter, ventricular tachycardia, and ventricular fibrillation. (wikipedia.org)
  • Class I agents are grouped by what effect they have on the Na+ channel, and what effect they have on cardiac action potentials. (wikipedia.org)
  • Antiarrhythmic agents may be an appropriate measure to treat cardiac arrhythmias resulting from doxepin overdose. (wikipedia.org)
  • It may be necessary to use antiarrhythmic agents for concomitant tachyarrhythmia. (medscape.com)
  • In individuals with significant tachyarrhythmias, amiodarone and other class III-type antiarrhythmic agents have also been used. (medscape.com)
  • citation needed] Some causes of tachycardia include: Adrenergic storm Alcohol Amphetamine Anaemia Antiarrhythmic agents Anxiety Atrial fibrillation Atrial flutter Atrial tachycardia AV nodal reentrant tachycardia Brugada syndrome Caffeine Cocaine Exercise Fear Fever Hypoglycemia Hypovolemia Hyperthyroidism Hyperventilation Infection Junctional tachycardia Methamphetamine Multifocal atrial tachycardia Nicotine Pacemaker mediated Pain Pheochromocytoma Sinus tachycardia Tricyclic antidepressants Wolff-Parkinson-White syndrome An electrocardiogram (ECG) is used to classify the type of tachycardia. (wikipedia.org)
  • Many attempts have been made to classify antiarrhythmic agents. (wikipedia.org)
  • The problem arises from the fact that many of the antiarrhythmic agents have multiple modes of action, making any classification imprecise. (wikipedia.org)
  • The five main classes in the Vaughan Williams classification of antiarrhythmic agents are: Class I agents interfere with the sodium (Na+) channel. (wikipedia.org)
  • The class I antiarrhythmic agents interfere with the sodium channel. (wikipedia.org)
  • ADVAIR HFA should be used for patients not adequately controlled on a long-term asthma control medication such as an inhaled corticosteroid (ICS) or whose disease warrants initiation of treatment with both an ICS and long-acting beta 2 -adrenergic agonist (LABA). (rxlist.com)
  • It has psychostimulant-like effects and its actions appear to be mediated by the dopaminergic and adrenergic systems. (wikipedia.org)
  • BMS-986121: μ-PAM BMS-986122: μ-PAM δ-PAM (see reference) Cannabidiol Tetrahydrocannabinol Sodium (Na+) List of opioids Adenosinergic Adrenergic Cannabinoidergic Cholinergic Dopaminergic GABAergic Glycinergic Histaminergic Melatonergic Monoaminergic Serotonergic Burford NT, Clark MJ, Wehrman TS, et al. (wikipedia.org)
  • Relative to other dopaminergic antiparkinsonian agents, pardoprunox is thought to have significantly less of a propensity for inducing certain side effects like dyskinesia and psychosis. (wikipedia.org)