Phenylalanine Hydroxylase: An enzyme of the oxidoreductase class that catalyzes the formation of L-TYROSINE, dihydrobiopterin, and water from L-PHENYLALANINE, tetrahydrobiopterin, and oxygen. Deficiency of this enzyme may cause PHENYLKETONURIAS and PHENYLKETONURIA, MATERNAL. EC 1.14.16.1.Phenylalanine: An essential aromatic amino acid that is a precursor of MELANIN; DOPAMINE; noradrenalin (NOREPINEPHRINE), and THYROXINE.Phenylketonurias: A group of autosomal recessive disorders marked by a deficiency of the hepatic enzyme PHENYLALANINE HYDROXYLASE or less frequently by reduced activity of DIHYDROPTERIDINE REDUCTASE (i.e., atypical phenylketonuria). Classical phenylketonuria is caused by a severe deficiency of phenylalanine hydroxylase and presents in infancy with developmental delay; SEIZURES; skin HYPOPIGMENTATION; ECZEMA; and demyelination in the central nervous system. (From Adams et al., Principles of Neurology, 6th ed, p952).Vasopressins: Antidiuretic hormones released by the NEUROHYPOPHYSIS of all vertebrates (structure varies with species) to regulate water balance and OSMOLARITY. In general, vasopressin is a nonapeptide consisting of a six-amino-acid ring with a cysteine 1 to cysteine 6 disulfide bridge or an octapeptide containing a CYSTINE. All mammals have arginine vasopressin except the pig with a lysine at position 8. Vasopressin, a vasoconstrictor, acts on the KIDNEY COLLECTING DUCTS to increase water reabsorption, increase blood volume and blood pressure.Hydroxylation: Placing of a hydroxyl group on a compound in a position where one did not exist before. (Stedman, 26th ed)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.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.Dihydralazine: 1,4-Dihydrazinophthalazine. An antihypertensive agent with actions and uses similar to those of HYDRALAZINE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p354)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.Phenylalanine Ammonia-Lyase: An enzyme that catalyzes the deamination of PHENYLALANINE to form trans-cinnamate and ammonia.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.Cholesterol, LDL: Cholesterol which is contained in or bound to low density lipoproteins (LDL), including CHOLESTEROL ESTERS and free cholesterol.Lipoproteins, LDL: A class of lipoproteins of small size (18-25 nm) and light (1.019-1.063 g/ml) particles with a core composed mainly of CHOLESTEROL ESTERS and smaller amounts of TRIGLYCERIDES. The surface monolayer consists mostly of PHOSPHOLIPIDS, a single copy of APOLIPOPROTEIN B-100, and free cholesterol molecules. The main LDL function is to transport cholesterol and cholesterol esters to extrahepatic tissues.Cholesterol, Dietary: Cholesterol present in food, especially in animal products.Renin: A highly specific (Leu-Leu) endopeptidase that generates ANGIOTENSIN I from its precursor ANGIOTENSINOGEN, leading to a cascade of reactions which elevate BLOOD PRESSURE and increase sodium retention by the kidney in the RENIN-ANGIOTENSIN SYSTEM. The enzyme was formerly listed as EC 3.4.99.19.Aldosterone: A hormone secreted by the ADRENAL CORTEX that regulates electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium.Methyldopa: An alpha-2 adrenergic agonist that has both central and peripheral nervous system effects. Its primary clinical use is as an antihypertensive agent.Renin-Angiotensin System: A BLOOD PRESSURE regulating system of interacting components that include RENIN; ANGIOTENSINOGEN; ANGIOTENSIN CONVERTING ENZYME; ANGIOTENSIN I; ANGIOTENSIN II; and angiotensinase. Renin, an enzyme produced in the kidney, acts on angiotensinogen, an alpha-2 globulin produced by the liver, forming ANGIOTENSIN I. Angiotensin-converting enzyme, contained in the lung, acts on angiotensin I in the plasma converting it to ANGIOTENSIN II, an extremely powerful vasoconstrictor. Angiotensin II causes contraction of the arteriolar and renal VASCULAR SMOOTH MUSCLE, leading to retention of salt and water in the KIDNEY and increased arterial blood pressure. In addition, angiotensin II stimulates the release of ALDOSTERONE from the ADRENAL CORTEX, which in turn also increases salt and water retention in the kidney. Angiotensin-converting enzyme also breaks down BRADYKININ, a powerful vasodilator and component of the KALLIKREIN-KININ SYSTEM.Sodium, Dietary: Sodium or sodium compounds used in foods or as a food. The most frequently used compounds are sodium chloride or sodium glutamate.Sodium: A member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23.Blood Pressure: PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.Plasma Volume: Volume of PLASMA in the circulation. It is usually measured by INDICATOR DILUTION TECHNIQUES.Guanethidine: An antihypertensive agent that acts by inhibiting selectively transmission in post-ganglionic adrenergic nerves. It is believed to act mainly by preventing the release of norepinephrine at nerve endings and causes depletion of norepinephrine in peripheral sympathetic nerve terminals as well as in tissues.Hypertension: Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.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.Product Surveillance, Postmarketing: Surveillance of drugs, devices, appliances, etc., for efficacy or adverse effects, after they have been released for general sale.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.Heart Atria: The chambers of the heart, to which the BLOOD returns from the circulation.Tachycardia, Sinus: Simple rapid heartbeats caused by rapid discharge of impulses from the SINOATRIAL NODE, usually between 100 and 180 beats/min in adults. It is characterized by a gradual onset and termination. Sinus tachycardia is common in infants, young children, and adults during strenuous physical activities.Tachycardia, Supraventricular: A generic expression for any tachycardia that originates above the BUNDLE OF HIS.Arrhythmias, Cardiac: Any disturbances of the normal rhythmic beating of the heart or MYOCARDIAL CONTRACTION. Cardiac arrhythmias can be classified by the abnormalities in HEART RATE, disorders of electrical impulse generation, or impulse conduction.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.Tachycardia: Abnormally rapid heartbeat, usually with a HEART RATE above 100 beats per minute for adults. Tachycardia accompanied by disturbance in the cardiac depolarization (cardiac arrhythmia) is called tachyarrhythmia.Tachycardia, Ventricular: An abnormally rapid ventricular rhythm usually in excess of 150 beats per minute. It is generated within the ventricle below the BUNDLE OF HIS, either as autonomic impulse formation or reentrant impulse conduction. Depending on the etiology, onset of ventricular tachycardia can be paroxysmal (sudden) or nonparoxysmal, its wide QRS complexes can be uniform or polymorphic, and the ventricular beating may be independent of the atrial beating (AV dissociation).Electrocardiography: Recording of the moment-to-moment electromotive forces of the HEART as projected onto various sites on the body's surface, delineated as a scalar function of time. The recording is monitored by a tracing on slow moving chart paper or by observing it on a cardioscope, which is a CATHODE RAY TUBE DISPLAY.Digitalis Glycosides: Glycosides from plants of the genus DIGITALIS. Some of these are useful as cardiotonic and anti-arrhythmia agents. Included also are semi-synthetic derivatives of the naturally occurring glycosides. The term has sometimes been used more broadly to include all CARDIAC GLYCOSIDES, but here is restricted to those related to Digitalis.Heart: The hollow, muscular organ that maintains the circulation of the blood.Anti-Arrhythmia Agents: Agents used for the treatment or prevention of cardiac arrhythmias. They may affect the polarization-repolarization phase of the action potential, its excitability or refractoriness, or impulse conduction or membrane responsiveness within cardiac fibers. Anti-arrhythmia agents are often classed into four main groups according to their mechanism of action: sodium channel blockade, beta-adrenergic blockade, repolarization prolongation, or calcium channel blockade.
(1/296) Neuroregulation by vasoactive intestinal peptide (VIP) of mucus secretion in ferret trachea: activation of BK(Ca) channels and inhibition of neurotransmitter release.

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)

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

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)

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

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)

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

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)

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

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)

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

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)

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

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)

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

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)

*  Phentolamine
It is important to note that phentolamine is not a first-line agent for this indication. Phentolamine should only be given to ... In response, the β1 adrenergic receptors on the heart increase its rate, contractility, and dromotropy, which help to offset ... Phentolamine (Regitine) is a reversible nonselective α-adrenergic antagonist. Its primary action is vasodilation due to α1 ... Phentolamine is marketed in the dental field as a local anesthetic reversal agent. Branded as OraVerse, it is a phentolamine ...
*  Colterol
A Beta-adrenergic Agent; Chemistry, Pharmacokinetics, Pharmacodynamics, Adverse Effects and Clinical Efficacy in Asthma". ...
*  Bitolterol
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 ...
*  Pain in amphibians
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 ...
*  Prenalterol
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 ...
*  1-Tetralone
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 ...
*  Labetalol
The minimum requirement for adrenergic agents is a primary or secondary amine separated from a substituted benzene ring by one ... Labetalol is highly selective for postsynaptic alpha1- adrenergic, and non-selective for beta-adrenergic receptors. It is about ... Labetalol is a dual alpha (α1) and beta (β1/β2) adrenergic receptor blocker and competes with other Catecholamines for binding ... Labetalol was the first drug created that combined both alpha- and beta- adrenergic receptor blocking properties. It was ...
*  Guanadrel
... 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 ...
*  Phenoxybenzamine
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. ...
*  Nebivolol
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 ...
*  Male contraceptive
Kjaergaard N, Kjaergaard B, Lauritsen JG; Kjaergaard; Lauritsen (June 1988). "Prazosin, an adrenergic blocking agent inadequate ...
*  Hordenine
... experiments on isolated tissue lead these investigators to conclude that hordenine was an indirectly acting adrenergic agent ... Although hordenine is capable of reacting with nitrosating agents (e.g. nitrite ion, NO2−) to form the carcinogen N- ...
*  List of MeSH codes (D16)
... adrenergic agents MeSH D27.505.519.625.050.100 --- adrenergic agonists MeSH D27.505.519.625.050.100.100 --- adrenergic alpha- ... adrenergic agents MeSH D27.505.696.577.050.100 --- adrenergic agonists MeSH D27.505.696.577.050.100.100 --- adrenergic alpha- ... anti-allergic agents MeSH D27.505.954.122 --- anti-infective agents MeSH D27.505.954.122.085 --- anti-bacterial agents MeSH ... antiviral agents MeSH D27.505.954.122.388.077 --- anti-retroviral agents MeSH D27.505.954.122.388.077.088 --- anti-hiv agents ...
*  Anxiogenic
... serotonergic agents such as mCPP and LY-293,284, adrenergic agents such as yohimbine, antipsychotics/dopamine antagonists such ... A number of agents are used to provoke anxiety (anxiogens) or panic (panicogens) in experimental models. Some of the most ... This effect is in contrast to anxiolytic agents, which inhibits anxiety. Together these categories of psychoactive compounds ...
*  Norfenefrine
... (INN) or meta-octopamine (3-octopamine), also known as 3,β-dihydroxyphenethylamine, is an adrenergic agent used as ... Macdonald F (1997). Dictionary of Pharmacological Agents. CRC Press. p. 104. ISBN 978-0-412-46630-4. Retrieved 24 April 2012. ...
*  Orthostatic hypotension
... can also be a side effect of alpha-1 blockers (alpha1 adrenergic blocking agents). Alpha1 blockers ...
*  Adrenergic agonist
An adrenergic agent is a drug, or other substance, which has effects similar to, or the same as, epinephrine (adrenaline). Thus ... the adrenergic receptors). Directly acting adrenergic agonists act on adrenergic receptors. All adrenergic receptors are G- ... An adrenergic agonist is a drug that stimulates a response from the adrenergic receptors. The five main categories of ... Indirectly acting adrenergic agonists affect the uptake and storage mechanisms involved in adrenergic signalling. Two uptake ...
*  Acrocyanosis
However, there is little, if any, empirical evidence that vasoactive drugs (α-adrenergic blocking agents or calcium channel ...
*  Benzodiazepine
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". ...
*  Restrictive cardiomyopathy
Digoxin, calcium channel blocking drugs and beta-adrenergic blocking agents provide little benefit, except in the subgroup of ... "Worsening of congestive heart failure in amyloid heart disease treated by calcium channel-blocking agents". American Journal of ...
*  Alpha-adrenergic agonist
An adrenergic alpha-agonist (or alpha-adrenergic agonists) are a class of sympathomimetic agents that selectively stimulates ... MeSH list of agents 82000316 Adrenergic alpha-Agonists at the US National Library of Medicine Medical Subject Headings (MeSH). ... Alpha blocker Adrenergic agonist Beta-adrenergic agonist Declerck I, Himpens B, Droogmans G, Casteels R (September 1990). "The ... The alpha-adrenergic receptor has two subclasses α1 and α2. Alpha 2 receptors are associated with sympatholytic properties. α ...
*  Bucumolol
... a beta-adrenergic blocking agent, on atrioventricular conduction in anesthetized dogs". Archives Internationales de ... Bucumolol is a beta-adrenergic antagonist. Nakayama, K; Oshima, T; Koike, H (1981). "Assessment of beta-blockade and the non- ...
*  Hyperhidrosis
... anxiolytic agents, adrenergic agonists, and cholinergic agonists. In people with a past history of spinal cord injuries ... Other anticholinergic agents that have tried to include propantheline bromide and benztropine.[citation needed] Injections of ... which cannot be managed by topical agents.[when?] A microwave-based device has been tried for excessive underarm perspiration ...
*  Garden tiger moth
Stein, J. M. (1975-09-15). "The effect of adrenaline and of alpha- and beta-adrenergic blocking agents on ATP concentration and ...
*  Naphazoline
It is a sympathomimetic agent with marked alpha adrenergic activity. It is a vasoconstrictor with a rapid action in reducing ...
*  List of investigational anxiolytics
... and α1-adrenergic receptor antagonist [12] Midomafetamine (MDMA; "ecstasy") - serotonin-norepinephrine-dopamine releasing agent ... α1-adrenergic, α2-adrenergic, and H1 receptor antagonist [10] Cyclobenzaprine (TNX-102) - undefined mechanism of action [11] ...
*  Lipoprotein lipase deficiency
... and b-adrenergic blocking agents. Gene therapy In 2012, the European Commission approved alipogene tiparvovec (Glybera), a gene ... Lipid lowering drugs Lipid-lowering agents such as fibrates and omega-3-fatty acids can be used to lower TG levels in LPLD, ... Additional measures are avoidance of agents known to increase endogenous triglyceride levels, such as alcohol, estrogens, ... certain antihypertensive agents, and paraproteinemic disorders) increases the possibility of LPL deficiency. In this instance ...
Treatment of renal hypertension. | Microbiology Department at UMass Amherst  Treatment of renal hypertension. | Microbiology Department at UMass Amherst
Adrenergic beta-Antagonists, Antihypertensive Agents, Diuretics, Humans, Hypertension, Renal, Kidney Diseases, Kidney Failure, ... We use them, alone or in combination, in the following line of order: diuretics, beta-adrenergic blockers, dihydralazine, ...
more infohttp://www.micro.umass.edu/faculty-and-research/publications/treatment-of-renal-hypertension
Naltrexone and Adrenergic Agents to Reduce Heroin Use in Heroin Addicts - Tabular View - ClinicalTrials.gov  Naltrexone and Adrenergic Agents to Reduce Heroin Use in Heroin Addicts - Tabular View - ClinicalTrials.gov
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 ...
more infohttps://clinicaltrials.gov/ct2/show/record/NCT00142948
Effects of adrenergic agents, vasopressin and ionophore A23187, on the phosphorylation of, and flux through, phenylalanine...  Effects of adrenergic agents, vasopressin and ionophore A23187, on the phosphorylation of, and flux through, phenylalanine...
Effects of adrenergic agents, vasopressin and ionophore A23187, on the phosphorylation of, and flux through, phenylalanine ... Effects of adrenergic agents, vasopressin and ionophore A23187, on the phosphorylation of, and flux through, phenylalanine ... Effects of adrenergic agents, vasopressin and ionophore A23187, on the phosphorylation of, and flux through, phenylalanine ... Effects of adrenergic agents, vasopressin and ionophore A23187, on the phosphorylation of, and flux through, phenylalanine ...
more infohttp://www.biochemj.org/content/219/1/87
Adrenergic Agents - Emergency Medicine - Barnard Health Care  Adrenergic Agents - Emergency Medicine - Barnard Health Care
b-adrenergic receptors are divided into two types b 1 and b2. ... b-adrenergic agonists are the preferred initial rescue ... b-adrenergic agonists are the preferred initial rescue medication for acute bronchospasm. b-adrenergic receptors are divided ... The b-adrenergic agonists used today are analogues of naturally occurring sympathomimetics ( Tab.l.e... 64-5). The ideal ... The most common side effect of b-adrenergic drugs is skeletal muscle tremor. Patients may also experience nervousness, anxiety ...
more infohttps://www.barnardhealth.us/emergency-medicine/adrenergic-agents.html
Adrenergic blocking agent - definition of adrenergic blocking agent by The Free Dictionary  Adrenergic blocking agent - definition of adrenergic blocking agent by The Free Dictionary
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. ...
more infohttps://www.thefreedictionary.com/adrenergic+blocking+agent
Adrenergic blocking agents | definition of adrenergic blocking agents by Medical dictionary  Adrenergic blocking agents | definition of adrenergic blocking agents by Medical dictionary
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 ...
more infohttps://medical-dictionary.thefreedictionary.com/adrenergic+blocking+agents
Pediatric Hypertrophic Cardiomyopathy Medication: Beta-Adrenergic Blocking Agents, Calcium Channel Blockers, Antiarrhythmics,...  Pediatric Hypertrophic Cardiomyopathy Medication: Beta-Adrenergic Blocking Agents, Calcium Channel Blockers, Antiarrhythmics,...
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 ...
more infohttps://emedicine.medscape.com/article/890068-medication
Exercise-Induced Anaphylaxis Medication: Sympathomimetic agents, Antihistamines, Beta2-adrenergic Agonist Agent, Corticosteroids  Exercise-Induced Anaphylaxis Medication: Sympathomimetic agents, Antihistamines, Beta2-adrenergic Agonist Agent, Corticosteroids
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 ...
more infohttps://emedicine.medscape.com/article/886641-medication
Synonyms and Antonyms for alpha-adrenergic blocking agent | Synonym.com  Synonyms and Antonyms for alpha-adrenergic blocking agent | Synonym.com
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 ...
more infohttp://www.synonym.com/synonyms/alpha-adrenergic%20blocking%20agent
Alpha-adrenergic blocking agent | definition of alpha-adrenergic blocking agent by Medical dictionary  Alpha-adrenergic blocking agent | definition of alpha-adrenergic blocking agent by Medical dictionary
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 ...
more infohttps://medical-dictionary.thefreedictionary.com/alpha-adrenergic+blocking+agent
Sympathomimetic Adrenergic Agents Category Listing & Drugs List on Catalog.md  Sympathomimetic Adrenergic Agents Category Listing & Drugs List on Catalog.md
Find your preferred Sympathomimetic Adrenergic Agents right here. ... Sympathomimetic Adrenergic Agents - Alpha- and Beta-Adrenergic ... Largest database of Sympathomimetic Adrenergic Agents listed for your easy reference. ... Miscellaneous Central Nervous System Agents (16913)*Alpha- and Beta-Adrenergic Agonists (5167)*Alpha-Adrenergic Agonists (250) ... Anorexigenic Agents and Respiratory and Cerebral Stimulants (517)*Anorectal Drug Products (5) ...
more infohttp://www.catalog.md/drugs-categories/sympathomimetic-adrenergic-agents/page-3.html
Sympathomimetic Adrenergic Agents Category Listing & Drugs List on Catalog.md  Sympathomimetic Adrenergic Agents Category Listing & Drugs List on Catalog.md
Find your preferred Sympathomimetic Adrenergic Agents right here. ... Sympathomimetic Adrenergic Agents - Alpha- and Beta-Adrenergic ... Largest database of Sympathomimetic Adrenergic Agents listed for your easy reference. ... Miscellaneous Central Nervous System Agents (16913)*Alpha- and Beta-Adrenergic Agonists (5167)*Alpha-Adrenergic Agonists (250) ... Anorexigenic Agents and Respiratory and Cerebral Stimulants (517)*Anorectal Drug Products (5) ...
more infohttp://www.catalog.md/drugs-categories/sympathomimetic-adrenergic-agents/page-6.html
Metaradrine
        -
        Adrenergic Agents,  Adrenergic alpha-Agonists,  Sympathomimetics,  Vasoconstrictor Agents,  ATC...  Metaradrine - Adrenergic Agents, Adrenergic alpha-Agonists, Sympathomimetics, Vasoconstrictor Agents, ATC...
Metaraminol acts on both α1-adrenergic receptors but appears to have no effect on β-adrenergic receptors. It acts by increasing ...
more infohttp://pharmacycode.com/Metaradrine.html
L-Metaraminol
        -
        Adrenergic Agents,  Adrenergic alpha-Agonists,  Sympathomimetics,  Vasoconstrictor Agents,  ATC...  L-Metaraminol - Adrenergic Agents, Adrenergic alpha-Agonists, Sympathomimetics, Vasoconstrictor Agents, ATC...
Metaraminol acts on both α1-adrenergic receptors but appears to have no effect on β-adrenergic receptors. It acts by increasing ...
more infohttp://pharmacycode.com/L-Metaraminol.html
Adrenergic neuronal blocking agent | Define Adrenergic neuronal blocking agent at Dictionary.com  Adrenergic neuronal blocking agent | Define Adrenergic neuronal blocking agent at Dictionary.com
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 ...
more infohttps://www.dictionary.com/browse/adrenergic-neuronal-blocking-agent
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. 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 ...
more infohttp://www.clinsci.org/content/48/s2/93s
Adrenergic neuron-blocking agent - definition of adrenergic neuron-blocking agent by The Free Dictionary  Adrenergic neuron-blocking agent - definition of adrenergic neuron-blocking agent by The Free Dictionary
adrenergic neuron-blocking agent synonyms, adrenergic neuron-blocking agent pronunciation, adrenergic neuron-blocking agent ... 2. One empowered to act for or represent another: an author's 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 ...
more infohttps://www.thefreedictionary.com/adrenergic+neuron-blocking+agent
Rapid screening of beta-adrenergic agents and related compounds in human urine for anti-doping purpose using capillary...  Rapid screening of beta-adrenergic agents and related compounds in human urine for anti-doping purpose using capillary...
Rapid screening of beta-adrenergic agents and related compounds in human urine for anti-doping purpose using capillary ... Mazzarino M, de la Torre X, Mazzei F, Botrè F. Rapid screening of beta-adrenergic agents and related compounds in human urine ... Rapid screening of beta-adrenergic agents and related compounds in human urine for anti-doping purpose using capillary ... This paper presents a capillary electrophoresis method, developed for the detection, in human urine, of beta-adrenergic agents ...
more infohttps://www.docphin.com/research/article-detail/4937274/PubMedID-19764051/Rapid-screening-of-beta-adrenergic-agents-and-related-compounds-in-human-urine-for-anti-doping-purpose-using-capillary-electrophoresis-with-dynamic-coating
Adrenergic neuron blocking agent | Article about adrenergic neuron blocking agent by The Free Dictionary  Adrenergic neuron blocking agent | Article about adrenergic neuron blocking agent by The Free Dictionary
The agent's 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 ...
more infohttps://encyclopedia2.thefreedictionary.com/adrenergic+neuron+blocking+agent
Cardiovascular adverse drug reaction associated with combined beta-adrenergic and calcium entry-blocking agents.  Cardiovascular adverse drug reaction associated with combined beta-adrenergic and calcium entry-blocking agents.
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 ...
more infohttp://www.biomedsearch.com/nih/Cardiovascular-adverse-drug-reaction-associated/10774785.html
  • The absence of secondary causes of severe hypertriglyceridemia (like e.g. diabetes, alcohol, estrogen-, glucocorticoid-, antidepressant- or isotretinoin-therapy, certain antihypertensive agents, and paraproteinemic disorders) increases the possibility of LPL deficiency. (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)
  • Lipid lowering drugs Lipid-lowering agents such as fibrates and omega-3-fatty acids can be used to lower TG levels in LPLD, however those drugs are very often not effective enough to reach treatment goals in LPLD patients. (wikipedia.org)
  • The mechanism of bronchodilator action of b-adrenergic drugs involves stimulation of the enzyme adenyl cyclase, which converts intracellular adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP). (barnardhealth.us)
  • Additional measures are avoidance of agents known to increase endogenous triglyceride levels, such as alcohol, estrogens, diuretics, isotretinoin, anidepressants (e.g. sertraline) and b-adrenergic blocking agents. (wikipedia.org)