One of the ADRENERGIC BETA-ANTAGONISTS used as an antihypertensive, anti-anginal, and anti-arrhythmic agent.
Compounds possessing both a hydroxyl (-OH) and an amino group (-NH2).
Drugs that inhibit the actions of the sympathetic nervous system by any mechanism. The most common of these are the ADRENERGIC ANTAGONISTS and drugs that deplete norepinephrine or reduce the release of transmitters from adrenergic postganglionic terminals (see ADRENERGIC AGENTS). Drugs that act in the central nervous system to reduce sympathetic activity (e.g., centrally acting alpha-2 adrenergic agonists, see ADRENERGIC ALPHA-AGONISTS) are included here.
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.
A moderately lipophilic beta blocker (ADRENERGIC BETA-ANTAGONISTS). It is non-cardioselective and has intrinsic sympathomimetic actions, but little membrane-stabilizing activity. (From Martindale, The Extra Pharmocopoeia, 30th ed, p638)
A beta-1 adrenergic antagonist that has been used in the emergency treatment of CARDIAC ARRYTHMIAS.
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.
A vasodilator with general properties similar to NITROGLYCERIN but with a more prolonged duration of action. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1025)
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.
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.
Isopropyl analog of EPINEPHRINE; beta-sympathomimetic that acts on the heart, bronchi, skeletal muscle, alimentary tract, etc. It is used mainly as bronchodilator and heart stimulant.
A beta-adrenergic antagonist used in the treatment of hypertension, angina pectoris, arrhythmias, and anxiety.
Drugs that selectively bind to and activate beta-adrenergic receptors.
AMINO ALCOHOLS containing the propanolamine (NH2CH2CHOHCH2) group and its derivatives.
Hydrogenated alprenolol derivative where the extra hydrogens are often tritiated. This radiolabeled form of ALPRENOLOL, a beta-adrenergic blocker, is used to label the beta-adrenergic receptor for isolation and study.
A non-selective beta-adrenergic antagonist with a long half-life, used in cardiovascular disease to treat arrhythmias, angina pectoris, and hypertension. Nadolol is also used for MIGRAINE DISORDERS and for tremor.
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.
A short-acting barbiturate that is effective as a sedative and hypnotic (but not as an anti-anxiety) agent and is usually given orally. It is prescribed more frequently for sleep induction than for sedation but, like similar agents, may lose its effectiveness by the second week of continued administration. (From AMA Drug Evaluations Annual, 1994, p236)
Drugs that bind to and block the activation of ADRENERGIC BETA-2 RECEPTORS.
An order of the class Amphibia, which includes several families of frogs and toads. They are characterized by well developed hind limbs adapted for jumping, fused head and trunk and webbed toes. The term "toad" is ambiguous and is properly applied only to the family Bufonidae.
A subclass of beta-adrenergic receptors (RECEPTORS, ADRENERGIC, BETA). The adrenergic beta-2 receptors are more sensitive to EPINEPHRINE than to NOREPINEPHRINE and have a high affinity for the agonist TERBUTALINE. They are widespread, with clinically important roles in SKELETAL MUSCLE; LIVER; and vascular, bronchial, gastrointestinal, and genitourinary SMOOTH MUSCLE.
An enzyme of the lyase class that catalyzes the formation of CYCLIC AMP and pyrophosphate from ATP. EC 4.6.1.1.
Physiological processes and properties of the RESPIRATORY SYSTEM as a whole or of any of its parts.
Process of administering an anesthetic through injection directly into the bloodstream.
A general class of ortho-dihydroxyphenylalkylamines derived from tyrosine.
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.

Identification of cardiac beta-adrenergic receptors by (minus) [3H]alprenolol binding. (1/127)

(Minus) [3-H] alprenolol, a potent beta-adrenergic antagonist, was used to identify binding sites in a fraction of canine cyocardium. Beta adrenergic agonists and antagonists compete for these binding sites in a manner which directly parallels their known affinity for the cardiac beta-adrenergic receptor. Thus, binding was highly stereo-specific, with the (minus) isomers of beta-adrenergic agonists or antagonists being at least two orders of magnitude more potent than were the (plus) isomers in competing for these sites. The order of potency for inhibition of binding by beta-adrenergic agonists was (minus) isoproterenol greater than (minus) epinephrine greater than (minus) norepinephrine. The dissociation constant (KD) of (minus) alprenolol for the beta-adrenergic receptors was 7-11 nM as determined independently by direct binding studies or by inhibition of isoproterenol-stimulated adenylate cyclase [ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1]. The beta-adrenergic antagonist (minus) propranolol also had high affinity for the binding sites (KD equals 12 nM). The physiologically inactive catechol-containing compounds pyrocatechol and (plus or minus) dihydroxymandelic acid, as well as the metabolite (plus or minus) normetanephrine, and the alpha-adrenergic antagonist phentolamine did not compete for the binding sites at a concentration of 160 muM. Binding was rapid (t1/2 less than 30 sec) and was rapidly reversible (t1/2 less than 15 sec). The binding sites were saturable and bound 0.35 pmol of (minus) [3-H] alprenolol per mg of membrane protein. These characteristics suggest that these binding sites represent the cardiac beta-adrenergic receptors.  (+info)

Catecholamine-induced subsensitivity of adenylate cyclase associated with loss of beta-adrenergic receptor binding sites. (2/127)

Injection of frogs with beta-adrenergic catecholamines for 1-24 hr produces marked subsensitivity of the erythrocyte membrane adenylate cyclase [ATP pyrophosphate-lyase (cyclizing); EC 4.6.1.1.] to in vitro stimulation by isoproterenol. The subsensitization is specific for catecholamine stimulation, since basal and fluoride-stimulated enzyme activity are unaffected. Maximum isoproterenol-stimulated adenylate cyclase activity declines by 75% in the isoproterenol-treated animals (P less than 0.001). The concentration of isoproterenol causing one-half maximal activation of adenylate cyclase, however, is unaltered. (-)[3H]Alprenolol, a potent competitive beta-adrenergic antagonist, was used to study directly the beta-adrenergic receptor binding sites in the erythrocyte membranes from control and subsensitized animals. A highly significant (P less than 0.005) 60% fall in the number of the beta-adrenergic receptor binding sites ("specific"(-)[3H]alprenolol binding sites) in the treated animals was found. The binding affinity of the sites was not markedly altered. These data suggest that beta-adrenergic catecholamines are able to regulate catecholamine sensitivity of tissues in vivo, by regulating the properties of the beta-adrenergic receptor binding sites.  (+info)

Rapid changes in rat pineal beta-adrenergic receptor: alterations in l-(3H)alprenolol binding and adenylate cyclase. (3/127)

The properties of the beta-adrenergic receptor which regulates adenylate cyclase [ATP pyrophosphate-lyase (cyclizing)8 EC 4.6.1.1] in the pineal gland are similar to the properties of the sites which specifically bind l-[3H]alprenolol, a potent beta-adrenergic antagonist. Stimulation of the beta-adrenergic receptor results in a 30-fold increase in the activity of N-acetyltransferase (= arylamine acetyltransferase; acetyl CoA:arylamine N-acetyltransferase, EC 2.3.1.5), an enzyme involved in the synthesis of thepineal hormone melatonin. In the normal diurnal light-dark cycle there is greater physiological stimulation of the beta-adrenergic receptor in the pineal during the night than during the day. Pineals from rats kept in constant light for 24 hr possess more hormone-sensitive adenylate cyclase and specifically bind more l-[3H]alprenolol than do pineals from rats kept in the dark overnight. When rats, exposed to light for 24 hr, are treated with the beat-adrenergic agonist isoproterenol, there is a rapid loss of both hormone-sensitive adenylate cyclase activity and specific l-[3H]alprenolol binding sites. There is no change in the affinity of adenylate cyclase for isoproterenol or for its substrate, ATP. Similarly, although there are fewer binding sites, there is no change in the affinity of the remaining sites for either agonist or antagonist. Inhibition of protein synthesis with cycloheximide does not affect the loss of either adenylate cyclase activity or specific binding sites. The data suggest that stimulation of the beta-adrenergic receptor causes a rapid decrease in the number of available receptors and in hormone-sensitive adenylate cyclase activity; conversely, lack of stimulation causes an increase in these parameters. It is suggested that these changes contribute to the phenomena of super- and subsensitivity in the pineal gland by regulating the capacity of the pineal to synthesize cyclic AMP in response to beta-adrenergic stimulation.  (+info)

Involvement of beta1- and beta2- but not beta3-adrenoceptor activation in adrenergic PYY secretion from the isolated colon. (4/127)

The secretion of PYY by endocrine L cells of the terminal gut is under the control of nutrients, the autonomic nervous system and hormones. Catecholamines, and the non-specific beta-adrenergic agonist isoproterenol induce PYY secretion from rat isolated colon or ileum. Because beta3-adrenergic receptors now appear to mediate many of the effects of catecholamines in the gastrointestinal tract, we investigated the involvement of beta1-, beta2-, and beta3-adrenoceptor stimulation in PYY secretion from the isolated, vascularly perfused rat colon. Infusion of 10(-6) M isoproterenol induced a transient increase in PYY secretion (from 36+/-4 to 87+/-20 fmol/2 min; n=7, P<0.05), that was abolished by a previous infusion of the beta1- and beta2-adrenergic blocker (and partial beta3-agonist) alprenolol (10(-6) M). The beta1-adrenergic agonist dobutamine and the beta-2 agonist terbutaline also (both at 10(-5) M) significantly stimulated PYY secretion, from 29+/-1 to 79+/-12 fmol/2 min and from 19+/-1 to 73+/-13 fmol/2 min respectively (n=7, P<0.05). Neither of the beta3-adrenergic agonists tested (BRL 37 344 (10(-5), 10(-6) M) and SR 58 611A (10(-6) M)) significantly stimulated PYY secretion, thus confirming the exclusive involvement of beta1- and beta2-receptors in beta-adrenergic agonist induced hormone secretion.  (+info)

Pharmacological analysis of dopamine action on the isolated dog atrium. (5/127)

The isolated right atrium of the dog was perfused with arterial blood introduced from a carotid artery of a support dog. The selective injection of dopamine, tyramine and norepinephrine into the cannulated sinus node artery induced dose-relatedly positive chronotropic and inotropic effects. However, for an equal increase in sinus rate, dopamine caused less increase in tension development than norepinephrine. Tyramine caused least increase in contractility. Effects induced by dopamine were not blocked by treatment with tetrodotoxin which blocked those induced by nicotine. Desmethylimipramine treatment significantly suppressed dopamine-induced effects and completely blocked tyramine-induced ones but rather enhanced norepinephrine-induced ones. Alprenolol inhibited effects of dopamine, tyramine and norepinephrine. From these results, it is concluded that positive chronotropic and inotropic effects of dopamine are partly due to tyramine-like effect which causes the release of norepinephrine from sympathetic storage sites.  (+info)

Maltodextrin-based proniosomes. (6/127)

Niosomes are nonionic surfactant vesicles that have potential applications in the delivery of hydrophobic or amphiphilic drugs. Our lab developed proniosomes, a dry formulation using a sorbitol carrier coated with nonionic surfactant, which can be used to produce niosomes within minutes by the addition of hot water followed by agitation. The sorbitol carrier in the original proniosomes was soluble in the solvent used to deposit surfactant, so preparation was tedious and the dissolved sorbitol interfered with the encapsulation of one model drug. A novel method is reported here for rapid preparation of proniosomes with a wide range of surfactant loading. A slurry method has been developed to produce proniosomes using maltodextrin as the carrier. The time required to produce proniosomes by this simple method is independent of the ratio of surfactant solution to carrier material and appears to be scalable. The flexibility of the proniosome preparation method would allow for the optimization of drug encapsulation in the final formulation based on the type and amount of maltodextrin. This formulation of proniosomes is a practical and simple method of producing niosomes at the point of use for drug delivery.  (+info)

Effect of chronic beta-adrenergic receptor blockade in congestive cardiomyopathy. (7/127)

Adrenergic beta-blocking agents were given to 7 patients with advanced congestive cardiomyopathy who had tachycardia at rest (98 plus or minus 13 beats/min). The patients were on beta-adrenergic receptor blockade for 2 to 12 months (average 5-4 months). One patient was given alprenolol 50 mg twice daily and the other patients were given practolol 50 to 400 mg twice daily. Virus infection had occurred in 6 of the patients before the onset of symptoms of cardiac disease. All patients were in a steady state or were progressively deteriorating at the start of beta-adrenergic receptor blockade. Conventional treatment with digitalis and diuretics was unaltered or reduced during treatment with beta-blocking agents. An improvement was seen in their clinical condition shortly after administration of the drugs. Continued treatment resulted in an increase in physical working capacity and a reduction of heart size. Noninvasive investigations including phonocardiogram, carotid pulse curve, apex cardiogram, and echocardiogram showed improved ventricular function in all cases. The present study indicates that adrenergic beta-blocking agents can improve heart function in at lease some patients with congestive cardiomyopathy. Furthermore, it is suggested that increased catecholamine activity may be an important factor for the development of this disease, as has been shown in animal experiments.  (+info)

Identification of beta-adrenergic receptors in human lymphocytes by (-) (3H) alprenolol binding. (8/127)

Human lymphocytes are known to posessess a catecholamine-responsive adenylate cyclase which has typical beta-adrenergic specificity. To identify directly and to quantitate these beta-adenergic receptors in human lymphocytes, (-) [3H] alprenolol, a potent beta-adrenergic antagonist, was used to label binding sites in homogenates of human mononuclear leukocytes. Binding of (-) [3H] alprenolol to these sites demonstrated the kinetics, affinity, and stereospecificity expected of binding to adenylate cyclase-coupled beta-adrenergic receptors. Binding was rapid (t1/2 less than 30 s) and rapidly reversible (t1/2 less than 3 min) at 37 degrees C. Binding was a saturable process with 75 +/- 12 fmol (-) [3H] alprenolol bound/mg protein (mean +/- SEM) at saturation, corresponding to about 2,000 sites/cell. Half-maximal saturation occurred at 10 nM (-) [3H] alprenolol, which provides an estimate of the dissociation constant of (-) [3H] alprenolol for the beta-adrenergic receptor. The beta-adrenergic antagonist, (-) propranolol, potently competed for the binding sites, causing half-maximal inhibition of binding at 9 nM. beta-Adrenergic agonists also competed for the binding sites. The order of potency was (-) isoproterenol greater than (-) epinephrine greater than (-)-norepinephrine which agreed with the order of potency of these agents in stimulating leukocyte adenylate cyclase. Dissociation constants computed from binding experiments were virtually identical to those obtained from adenylate cyclase activation studies. Marked stereospecificity was observed for both binding and activation of adenylate cyclase. (-)Stereoisomers of beta-adrenergic agonists and antagonists were 9- to 300-fold more potent than their corresponding (+) stereoisomers. Structurally related compounds devoid of beta-adrenergic activity such as dopamine, dihydroxymandelic acid, normetanephrine, pyrocatechol, and phentolamine did not effectively compete for the binding sites. (-) [3H] alprenolol binding to human mononuclear leukocyte preparations was almost entirely accounted for by binding to small lymphocytes, the predominant cell type in the preparations. No binding was detectable to human erythrocytes. These results demonstrate the feasibility of using direct binding methods to study beta-adrenergic receptors in a human tissue. They also provide an experimental approach to the study of states of altered sensitivity to catecholamines at the receptor level in man.  (+info)

TY - JOUR. T1 - Electrophysiological effects of alprenolol on depressed canine myocardium. AU - Guse, Paul A.. AU - Gaide, Marion S.. AU - Myerburg, Robert J.. AU - Epstein, Kristina. AU - Gelband, Henry. AU - Bassett, Arthur L.. PY - 1980/11. Y1 - 1980/11. N2 - The electrophysiological effects of the β-adrenergic antagonist, alprenolol, were compared in normal and depressed canine myocardium. Both (+) and (±)-alprenolol (5 x 10 -6 and 10 -5 mol.litre -1) decreased action potential amplitude and V̇max in Purkinje fibres superfused with Tyrodes solution in tissue bath. These concentrations shortened action potential duration and effective refractory period of Purkinje fibres but prolonged those of ventricular muscle. Alprenolol more markedly decreased V(max) and sometimes prevented action potential propagation in Purkinje fibres overlying infarcted regions. Similar depressant actions were noted in Purkinje fibres depolarised by exposure to 9 mmol.litre -1 K +. Depolarised and diseased ...
Alprenolol: Search drug information, interaction, images & medical diagnosis. The most comprehensive database of medicines available in China, Hong Kong, T...
hypothetical protein, 5-ht7, 5Ht7, 5-HT-7, 5-HT7 receptor, 5-HT receptor 7a, 5-HT-X, 5-hydroxytryptamine 7 receptor, 5-hydroxytryptamine7 receptor, 5-hydroxytryptamine (serotonin) receptor 7, 5-hydroxytryptamine (serotonin) receptor 7 (adenylate cyclase-coupled), 5-hydroxytryptamine (serotonin) receptor 7, adenylate cyclase-coupled, Anapl_03536, AS27_02610, AS28_04456, CB1_000689030, D623_10028851, GPRFO, H920_08680, high affinity serotonin receptor (5HT7), I79_004939, M91_18026, M959_09888, MDA_GLEAN10014860, N300_07498, N301_10640, N302_13493, N305_11464, N306_13870, N307_06146, N308_09036, N330_05281, N331_09625, N334_00682, PAL_GLEAN10018375, serotonin 5-hydroxytryptamine 7-a receptor, serotonin receptor 7, Y1Q_023580, Y956_01514, htr7 ...
Seven healthy volunteers showing a fourteenfold range in steady-state plasma concentrations on oral alprenolol (200 mg b.i.d.) were investigated by administration of 5 mg of the drug intravenously and then 50, 100, 150, and 200 mg as single oral doses. The rank order for individual steady-state plasma concentrations was the same as that for the relative bioavailability of the 200 mg dose. The area under the plasma concentration-time curve showed a nonlinear increase with the dose. As the relative availability was a good predictor of steady state while clearance after intravenous administration was not, it was concluded that differences in first-pass elimination markedly contribute to the interindividual variability in steady state plasma concentrations. After pentobarbital treatment, the area under the plasma concentration curve of the 200 mg dose was decreased to 32% and 59% of the pretreatment values in two subjects, but there was no change in the plasma half-life of alprenolol. This indicates
HEK293T-HuHTR7-FLAG cell line is a hypotriploid human cell line, which has been transfected with a human 5-hydroxytryptamine (serotonin) receptor 7, adenylate cyclase-coupled (HTR7) tagged in the N-terminus with FLAG to allow stably express of the human HTR7 tagged in the N-terminus with FLAG. It is an example of a cell line transfected using our proprietary CBTGS gene screening and amplification system.
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β2-Adrenergic receptors (β2AR) play important regulatory roles in a variety of cells and organ systems and are important therapeutic targets in the treatment of airway and cardiovascular disease. Prolonged use of β-agonists results in tolerance secondary to receptor down-regulation resulting in reduced therapeutic efficiency. The purpose of this work is to evaluate the signaling capabilities of the β2AR expressed by a recombinant adeno-associated viral (AAV) vector that also included an enhanced green fluorescent protein (EGFP) gene (AAV-β2AR/EGFP). By epifluorescence microscopy, ~40% of infected HEK 293 cells demonstrated EGFP expression. β2AR density measured with [3H]dihydroalprenolol ([3H]DHA) increased either 13- or 77-fold in infected cells compared to mock infected controls depending on the culture conditions used. The [3H]DHA binding was to a single receptor population with a dissociation constant of 0.42 nM, as would be expected for wild-type β2AR. Agonist competition assays with [3H]DHA
Antianginal drugs, including nitrates, beta-blockers, and calcium channel blockers, are used in the treatment of angina pectoris. Here is the latest research on their use and their mechanism of action. ...
Keywords: Sorbitol Based Proniosomes PermeabilityOral Cephlosporin. Introduction . absorbing the liquid with the tip of a piece of filter paper and sample was International Journal of Research in Pharmaceutical…25 Jun 2017 Publish your
We previously reported that Asn312 of the beta 2-adrenergic receptor and Asn385 in the homologous position in the 5-hydroxytryptamine1A receptor are important for binding to a class of beta-adrenergic receptor antagonists including propranolol and alprenolol. We proposed that the asparagine may be forming a hydrogen bond with the phenoxy oxygen common to these ligands. To further test this hypothesis we made alanine, threonine, phenylalanine, and glutamine substitutions at position 312 in the beta 2-adrenergic receptor. We observed that substitution with amino acids that permit formation of hydrogen bonds (threonine and glutamine) supported binding to aryloxyalkylamines, whereas substitution with amino acids that cannot form hydrogen bonds (alanine and phenylalanine) did not permit binding to these compounds. We were surprised to find that two of these substitutions led to an increase in affinity for alpha-adrenergic ligands. Substitution with glutamine and threonine at position 312 led to a ...
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0214]2-adrenergic receptor numbers were measured in asthmatic mice as follows. Asthmatic mice (ovalbumin-challenged) were treated as follows: Ctrl, no drug treatment with methacholine challenge; salbutamol, a short-acting β2 agonist; carvedilol, a β1, β2 non-selective inverse agonist with α1-adrenergic antagonist activity; nadolol, a highly specific, hydrophilic β1, β2 non-selective inverse agonist; and alprenolol, a β-adrenergic antagonist. Drug treatments were either a single treatment 15 minutes prior to methacholine challenge or ongoing for 28 days (salbutamol was delivered continuously via a subcutaneous osmotic minipump and alprenolol, carvedilol, and nadolol were in animal chow). Mice were sacrificed and lung membranes were isolated as follows. Frozen lung tissue was homogenized in an ice-cold buffer containing 0.32 M sucrose and 25 mM Tris (pH 7.4) using a polytron (Pro 200, Pro Scientific, Inc.). The homogenate was centrifuged at 1000×g for 10 min at 4° C. The resulting ...
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Sobolev A., Rosenkranz A., Kazarov A. A study of mechanisms of post-irradiation changes in adenylate-cyclase activity // International journal of radiation biology and related studies in physics, chemistry, and medicine. - 1983. - Vol. 44, no. 1. - P. 31-39. Hormone-stimulated adenylate-cyclase activity (via beta-adrenergic receptors) is reduced after in vitro irradiation of plasma membranes of frog erythrocytes, at a dose (650 Gy) which does not change the number of beta-adrenergic receptors but causes an oxidative degradation of membrane lipids. Peroxidation of membrane lipids without irradiation also results in a lesser stimulation of adenylate cyclase by the beta-agonist. A possible mechanism of change in adenylate-cyclase functioning is discussed. [ DOI ...
To more fully characterize the alterations in myocardial adrenergic and cholinergic receptors induced by the diabetic state, we investigated the binding characteristics of (-) [3H] dihydroalprenolol to beta adrenergic receptors (bAR), [3H] prazosin to alpha adrenergic receptors (aAR), and [3H] quinuclidinyl-benzilate to muscarinic cholinergic receptors (MCR) in myocardial membranes derived from rats 8 wk after treatment with streptozotocin. We also studied an equal number of animals from three control groups: free-eating nondi-abetics, pair-weighted nondiabetics, and streptozoto-cin-treated animals treated daily with insulin.. Diabetic hearts demonstrated 27% fewer bAR (P , 0.01) and 31% fewer aAR (P , 0.01) than free-eating controls, without changes in MCR, and without changes in antagonist affinity, agonist affinity, or agonist slope factor (pseudo-Hill coefficient) for any class of receptors. Food restriction had no effect on receptor characteristics, and treatment of diabetic rats with ...
Whether or not youre coping with the FAA (Federal Aviation Administration) or a RPIC (Distant Pilot In Command), its vital to know what the handfuls of acronyms in U.S. aerospace imply. Right heres a rundown of the most typical ones youll come throughout. AAO: Acronym for
Treatment of rats with chemical carcinogens, including 2-acetylaminofluorene (2-AAF), leads to a strong increase in the hepatic catecholamine-sensitive adenylate cyclase activity. The present study was undertaken to investigate the mechanism for the development of this increase. We report that hepatocytes isolated from rats which had been fed 2-AAF (0.025% w/w) for 8-12 weeks had an increased number of β-adrenoceptors, as determined by [3H]dihydroalprenolol binding to whole cells and [125I]iodocyanopindolol binding to washed particles. For both ligands the number of binding sites was about 4-fold higher in hepatocytes from 2-AAF-treated rats than in those from controls. The adenylate cyclase activity of the carcinogen-fed animals showed both a general increase manifested in the basal level (2-fold) and in the activities obtained by stimulation with guanine nucleotides (2-3-fold), cholera toxin (1.5-fold), and glucagon (1.3-fold) and a selective, larger increase in the β-adrenoceptor-linked ...
Studies conducted in our laboratory have demonstrated that activated immune cells produce a soluble inhibitor(s) of cardiac myocyte contractile and cyclic AMP (cAMP) responses to beta-adrenergic stimulation. To examine the mechanism of this effect, metabolic assays were conducted on cultured rat cardiac myocytes incubated in the presence and absence of supernatants harvested from rat activated splenocyte cultures. Intracellular cAMP accumulation in response to isoproterenol was inhibited by up to 74% in a dose-dependent fashion by conditioned media containing soluble cytokines from activated immune cells. By use of myocyte cultures in which contaminating nonmyocyte proliferation was inhibited by nonlethal irradiation, this phenomenon was shown to be independent of mitogenic effects. Isobutylmethylxanthine, a phosphodiesterase inhibitor, did not ablate cytokine-induced inhibition of cAMP accumulation. Parameters of beta-adrenergic receptor binding and affinity were also unaffected. cAMP ...
Long-term administration of imipramine caused a decrease in serotonin2 receptor binding in rat brain cerebral cortex, an effect that was abolished by ovariectomy. In contrast, ovariectomy had no effect on imipramine-induced decreases in hippocampal serotonin or in cerebral cortical and hippocampal beta-adrenergic receptor binding. Administration of estradiol or progesterone separately or in combination reestablished the effect of imipramine treatment on cortical serotonin2 receptors. These results suggest that ovarian steroids may play an important, but subtle, role in the neurochemical and perhaps clinical response to this drug. ...
The effects of various adrenergic beta receptor agonists and antagonists on lipolysis (measured as glycerol release) in human adipose tissue in vitro were studied. Of the agonists investigated, the potency rank order was isoproteronol greater than norepinephrine greater than salbutamol. Adrenergic beta receptor blocking drugs inhibited catecholamineinduced lipolysis competitively. Propranolol was the overall most effective compound, followed by metoprolol, alprenolol and practolol, whereas butoxamine and H35/25 were weak inhibitors. The results indicate that the adrenergic reciptor mediating lipolysis in human adipose tissue is of type beta-1. Basal and theophylline-induced lipolysis was reduced when higher concentrations of these drug were used. ...
The structure-activity relationships were determined for adrenergic compounds which either activated or blocked the activation of a partially purified adenyl cyclase isolated from frog erythrocytes. The results suggested that the presence of a β-hydroxyl group was essential for activity and that the potency of agonists as well as antagonists increased with the size of the substituent group of the amino nitrogen. In addition to the requirements for receptor affinity, compounds with intrinsic activity (agonists) had to have either OH or CH2OH substituents in both the m- and p-positions of the benzene ring. Since these structural requirements agreed well with those reported for intact tissue preparations, utilization of this relatively simple, cell-free preparation of adenyl cyclase may be a useful method for studying compounds with beta-adrenengic activity and for further defining the chemical nature of a beta-adrenergic receptor.. ...
The effects of dietary fats consisting of different fatty acids on lipolytic activity and body fat accumulation were studied in rats. Sprague-Dawley male rats were meal-fed an isoenergetic diet based on either beef tallow or safflower oil for 8 weeks. Lipolytic activities in epididymal and subcutaneous adipose tissues were lower in the beef tallow diet group than in the safflower oil diet group. Body fat accumulation was greater in rats fed the beef tallow diet versus the safflower oil diet. Norepinephrine (NE) turnover rates used as an index of sympathetic activities in adipose tissues were lower in the beef tallow diet group. beta-Adrenergic receptor binding was determined with [3H]dihydroalprenolol. Binding affinities of beta-receptors in adipose tissues were significantly lower in the beef tallow diet group. Membrane fluidities of adipose tissues were also lower in the beef tallow diet group. Membrane fluidities were correlated with the affinities of the beta-receptor. We believe from these ...
The effects of dietary fats consisting of different fatty acids on lipolytic activity and body fat accumulation were studied in rats. Sprague-Dawley male rats were meal-fed an isoenergetic diet based on either beef tallow or safflower oil for 8 weeks. Lipolytic activities in epididymal and subcutaneous adipose tissues were lower in the beef tallow diet group than in the safflower oil diet group. Body fat accumulation was greater in rats fed the beef tallow diet versus the safflower oil diet. Norepinephrine (NE) turnover rates used as an index of sympathetic activities in adipose tissues were lower in the beef tallow diet group. beta-Adrenergic receptor binding was determined with [3H]dihydroalprenolol. Binding affinities of beta-receptors in adipose tissues were significantly lower in the beef tallow diet group. Membrane fluidities of adipose tissues were also lower in the beef tallow diet group. Membrane fluidities were correlated with the affinities of the beta-receptor. We believe from these ...
Glomerular filtration rate and renal plasma flow in patients with essential hypertension before and after tratment with alprenolol. ...
Chlordimeform (N(4-chloro-o-tolyl)-N, N-dimethylformamidine; CDM) is a formamidine insecticide/acaricide whose major active metabolite is its N-monomethyl analog, desmethylchlordimeform, (DCDM). While their pesticidal action in invertebrates appears to be related to activation of octopamine receptors, their mechanism of action in mammals has not been established. Because of similarities between octopamine and adrenergic receptors and suggestions of CDM and DCDM action on adrenoceptors, the in vitro interactions of CDM and DCDM with adrenoceptors were studied. In mouse brain membrane preparations CDM inhibited the binding of [3H]-clonidine to alpha2- adrenoceptors and of [3H]-WB4101 to alpha1-adrenoceptors with IC50 values of 18.2 and 87 μM, respectively. DCDM was a much more potent inhibitor, with IC50 values toward alpha2−, and alpha1-adrenoceptors of 44 nM and 1 μM, respectively. Both compounds were only weak inhibitors of the binding of [3H]-dihydroalprenolol to beta-adrenoceptors and of [3H]
Synonyms for beta-adrenergic blocking agent in Free Thesaurus. Antonyms for beta-adrenergic blocking agent. 3 synonyms for beta-adrenergic blocking agent: beta blocker, beta-adrenergic blocker, beta-blocking agent. What are synonyms for beta-adrenergic blocking agent?
Combining with epinephrine or norepinephrine to initiate a change in cell activity via activation of a G protein, with pharmacological characteristics of beta-adrenergic receptors; the activity involves transmitting the signal to the Gs alpha subunit of a…
Evening, Drinkers. Well, that was terrible. Truly just awful. I mean, thank god for beer and having a friends to watch movies with (thanks Anne!) because otherwise I think I would have just turned Mars Attacks! off. Without exaggeration or hyperbole, this was the worst movie Ive watched for BAAM. Keep in mind that this is…
January 27, 2012 , 3:12 , Public Domain Welcome to the West Wing Week, your guide to everything thats happening at 1600 Pennsylvania Ave. This week, the President prepared for and delivered his State of the Union Address, welcomed the Boston Bruins to the White House, and took his message West to Iowa, Arizona, Nevada, and Colorado. Thats January 20th to January 26th or The Special State of the Union Edition of 2012.. ...
We have recently described the affinity chromatography purification of the turkey erythrocyte beta-adrenergic receptor. The minute amounts obtained initially precluded extensive biochemical characterization. To improve the yield of the receptor, the erythrocyte membranes have been prepared by a new method. This procedure resulted in a 10-fold higher receptor density in comparison with the membrane preparation used previously. The new membranes also contained a catecholamine-sensitive guanine triphosphatase and an adenylate cyclase sensitive to Gpp(NH)p and l-epinephrine. Solubilization by a double digitonin extraction resulted in a preparation containing 4-6 pmoles of 3H-dihydroalprenolol binding sites per mg of membrane protein. A single step of affinity chromatography on alprenolol-sepharose of the soluble digitonin extract resulted in an additional 1,000-fold purification of the receptor. The overall purification factor was 20,000 relative to the binding activity of the crude membrane ...
TY - JOUR. T1 - Skin fibroblast beta-adrenergic receptor function in manie-depressive illness. AU - Berrettini, Wade H.. AU - Bardakjian, Josiane. AU - Cappellari, Charles B.. AU - Barnett, Arthur L.. AU - Albright, Allen. AU - Nurnberger, John I.. AU - Gershon, Elliot S.. PY - 1987/12. Y1 - 1987/12. N2 - Beta-adrenergic receptor function was assessed in cultured skin fibroblasts obtained from bipolar patients and normal volunteers by measurement of the cyclic adenosine monophosphate (cAMP) response to isoproterenol. No group differences were observed. To assess regulation of receptor desensitization, fibroblasts were incubated for 24 hr with isoproterenol, and then the cAMP response to isoproterenol was determined. Subsensitivity to rechallenge with isoproterenol did not distinguish bipolar patients from controls.. AB - Beta-adrenergic receptor function was assessed in cultured skin fibroblasts obtained from bipolar patients and normal volunteers by measurement of the cyclic adenosine ...
Desipramine-yohimbine combination treatment of refractory depression. Implications for the beta-adrenergic receptor hypothesis of antidepressant action ...
RecName: Full=Adenylate cyclase type 6; EC=4.6.1.1;AltName: Full=Adenylate cyclase type VI;AltName: Full=ATP pyrophosphate-lyase 6;AltName: Full=Adenylyl cyclase 6;AltName: Full=Ca(2+)-inhibitable adenylyl ...
RecName: Full=Adenylate cyclase type 2; EC=4.6.1.1;AltName: Full=Adenylate cyclase type II;AltName: Full=ATP pyrophosphate-lyase 2;AltName: Full=Adenylyl cyclase ...
Timolol is a nonselective beta-adrenergic antagonist given in an eye drop solution to reduce intraocular pressure, or buy cialis - http://ci
TY - JOUR. T1 - Multiple forms of brain adenylate cyclase. T2 - Stimulation by Mn2+. AU - Malamuda, Daniel F.. AU - DiRusso, Concetta C.. AU - Aprille, June R.. PY - 1977/11/23. Y1 - 1977/11/23. N2 - Mn2+-stimulated adenylate cyclase (ATP pyrophosphate-lyase-(cyclizing), EC 4.6.1.1) activity in detergent solubilized preparations from mouse brain. While NaF-stimulated activity was decreased by both solubilization and storage at 0-4°C, the ability of the enzyme to be stimulated by Mn2+ was maintained for up to one week. By including Mn+ in the assay of adenylate cyclase in gel fractions after isoelectric focusing, two distinct peaks of enzyme activity (pI1 = 5.8, pI2 = 6.4) were detected, suggesting the existence of more than one type of catalytic subunit in mouse brain cell membranes.. AB - Mn2+-stimulated adenylate cyclase (ATP pyrophosphate-lyase-(cyclizing), EC 4.6.1.1) activity in detergent solubilized preparations from mouse brain. While NaF-stimulated activity was decreased by both ...
RECONSTITUTION OF BETA-ADRENERGIC RECEPTORS INTO LIPID VESICLES - AFFINITY-CHROMATOGRAPHY PURIFIED RECEPTORS CONVEY CATECHOLAMINE RESPONSIVENESS TO A HETEROLOGOUS ADENYLATE-CYCLASE SYSTEM
A non-selective beta-adrenergic antagonist with a long half-life, used in cardiovascular disease to treat arrhythmias, angina pectoris, and hypertension. Nadolol is also used for MIGRAINE DISORDERS and for tremor ...
Cardivas is a brand name for Carvedilol, which is a vasodilating non-selective beta-blocking agent with antioxidant properties. Carvedilol reduces the peripheral vascular resistance through...
Adrenergic beta-blocking agents were given to 7 patients with advanced congestive cardiomyopathy who had tachycardia at rest (98 plus or minus 13 beats/min). The patients were on beta-adrenergic receptor blockade for 2 to 12 months (average 5-4 months). One patient was given alprenolol 50 mg twice daily and the other patients were given practolol 50 to 400 mg twice daily. Virus infection had occurred in 6 of the patients before the onset of symptoms of cardiac disease. All patients were in a steady state or were progressively deteriorating at the start of beta-adrenergic receptor blockade. Conventional treatment with digitalis and diuretics was unaltered or reduced during treatment with beta-blocking agents. An improvement was seen in their clinical condition shortly after administration of the drugs. Continued treatment resulted in an increase in physical working capacity and a reduction of heart size. Noninvasive investigations including phonocardiogram, carotid pulse curve, apex cardiogram, ...
Hickie JB (1970). "Alprenolol ("aptin") in angina pectoris. A double-blind multicentre trial". Med. J. Aust. 2 (6): 268-72. doi ... Alprenolol, or alfeprol, alpheprol, and alprenololum (Gubernal, Regletin, Yobir, Apllobal, Aptine, Aptol Duriles), is a non- ...
It is a prodrug to alprenolol. Prokai L, Wu WM, Somogyi G, Bodor N (May 1995). "Ocular delivery of the beta-adrenergic ... antagonist alprenolol by sequential bioactivation of its methoxime analogue". Journal of Medicinal Chemistry. 38 (11): 2018-20 ...
... alprenolol binding". The Journal of Clinical Investigation. 57 (1): 149-155. doi:10.1172/JCI108254. PMC 436634. PMID 1245597. ...
When the extra hydrogen atoms are tritium, it is a radiolabeled form of alprenolol, which is used to label beta-adrenergic ... Dihydroalprenolol (DHA) is a hydrogenated alprenolol derivative that acts as a beta-adrenergic blocker. ...
... alprenolol (INN) alprostadil (INN) alrestatin (INN) Alrex alsactide (INN) Altace (Pfizer/Sanofi-Aventis) Altamist altanserin ( ...
The molecular formula C15H23NO2 (molar mass : 249.34 g/mol) may refer to: Alprenolol Castoramine, an alkaloid found in ...
Solabegron Terbutaline Tretoquinol Tulobuterol Xamoterol Zilpaterol Zinterol Acebutolol Adaprolol Adimolol Afurolol Alprenolol ...
Beta blockers Non-selective agents Alprenolol Bucindolol Carteolol Carvedilol (has additional α-blocking activity) Labetalol ( ...
ERK1/2 preferring agonist Alprenolol AV-965 Binospirone (postsynaptic 5-HT1A) BMY-7,378 Cannabigerol Cyanopindolol ...
... alprenolol MeSH D02.092.063.624.698.055.200 - dihydroalprenolol MeSH D02.092.063.624.698.070 - atenolol MeSH D02.092.063.624. ... alprenolol MeSH D02.033.100.624.058.200 - dihydroalprenolol MeSH D02.033.100.624.085 - atenolol MeSH D02.033.100.624.102 - ... alprenolol MeSH D02.033.755.624.058.200 - dihydroalprenolol MeSH D02.033.755.624.085 - atenolol MeSH D02.033.755.624.102 - ...
C07AA01 Alprenolol C07AA02 Oxprenolol C07AA03 Pindolol C07AA05 Propranolol C07AA06 Timolol C07AA07 Sotalol C07AA12 Nadolol ...
The molecular formula C15H22N2O2 may refer to: Alprenoxime, a beta blocker and prodrug to alprenolol Mepindolol, a non- ...
Alprenolol is no longer marketed by AstraZeneca, but may still be available in generic varieties. ... The metabolism of Alprenolol can be increased when combined with Abatacept.. Abiraterone. The metabolism of Alprenolol can be ... Alprenolol is nonpolar and hydrophobic, with low to moderate lipid solubility. Alprenolol has little to no intrinsic ... The metabolism of Alprenolol can be decreased when combined with Acetaminophen.. Acetazolamide. The risk or severity of adverse ...
During the extensive two-year review process for the 2021 version of the Code, WADA received considerable stakeholder feedback related to drugs of abuse where it was felt that the use of some substances included in the Prohibited List was often unrelated to sport practice. Accordingly, Article 4.2.3 was added to the 2021 Code defining Substances of Abuse as those "Prohibited Substances which are specifically identified as Substances of Abuse on the Prohibited List because they are frequently abused in society outside of the context of sport.". In this context, cocaine, diamorphine (heroin), methylenedioxymethamphetamine (MDMA/"ecstasy") and tetrahydrocannabinol (THC) are designated as Substances of Abuse. These 4 substances are prohibited in competition but sometimes their use out-of-competition can be detected in-competition and lead to an Adverse Analytical Finding. If the athlete can demonstrate that the use of any of these four substances was out-of -competition and unrelated to sport ...
alprenolol (beta-blocker) * mianserin (tetracyclic antidepressant) * phenformin (antidiabetic) * tropisetron (5-HT3 receptor ...
ANTI-ALPRENOLOL ANTIBODIES IN THE RABBIT - A NEW PROBE FOR THE STUDY OF BETA-ADRENERGIC-RECEPTOR INTERACTION CIRCULATION ... We immunized rabbits with an antigen prepared by covalent linkage of alprenolol, a beta-adrenergic receptor antagonist, to ... After 6 mo, antisera exhibited antiidiotypic activity inhibiting [3H]alprenolol binding to the original antibody and to rabbit ... Those antisera demonstrating the most potent antiidiotypic activity also blocked [3H]alprenolol binding to the beta-adrenergic ...
D12.776.377.715.85.90 Alprenolol D2.33.100.624.58 D2.33.755.624.58 Ammonium Chloride D1.625.75.25 D1.625.62.249 Ammonium ...
... alprenolol, [3H]WB-4101 and [ [3H]clonidine. Furthermore, the effects of adrenalectomy cannot be accounted for by a shift in ...
Alprenolol - Preferred Concept UI. M0000809. Scope note. One of the ADRENERGIC BETA-ANTAGONISTS used as an antihypertensive, ... alprenolol. Scope note:. Uno de los ANTAGONISTAS BETA-ADRENÉRGICOS utilizado como agente antihipertensor, antianginoso y ... Alprenolol Hydrochloride. Aptin. Aptin Duriles. Aptin-Duriles. AptinDuriles. Aptina. Aptine. H 56 28. H-56-28. H5628. ...
Alprenolol measurement (procedure). Code System Preferred Concept Name. Alprenolol measurement (procedure). Concept Status. ...
7-amino-clonazepam. 7-amino-flunitrazepam. Acepromethazine. Acetyl salicylic acid (aspirin). Mefenamic acid. Vvalproic acid. Alimemazine. Alprazolam. Amisulpride. Amitriptyline. Atropine Bromazepam. Butabarbital. Carbamazepine. Chlorpheniramine. Citalopram. Clobazam. Clonazepam. Clonidine. Cyamemazine. Diazepam. Diclofenac. Digitoxin. Digoxin. Diphenhydramine. Domperidone. Dosulepin. Dothiepin. Doxylamine. Flunitrazepam. Fluoxetine ...
Antagonists: Acebutolol • Adaprolol • Adimolol • Afurolol • Alprenolol • Alprenoxime • Amosulalol • Ancarolol • Arnolol • ...
Alprenolol. Naldolol. Propanolol. Atenolol. Oxprenolol. Sotalol. Opiate/starke Analgetika. Codein. Morphin. Pethidin. ...
39) An 11 year old boy was brought to the emergency by some of his friends because he started going crazy after eating seeds from a plant while trying to get high the boy was incoherent. His skin was hot and dry. His pupils were dilated and unresponsive to light. Pulse is 150 min and rectal temperature is 40 C the presumptive diagnosis was drug toxicity due to the ingestion of a compound similar to ...
... alprenolol = pindolol.;Species reactivity: Human;Application: ;Assay info: Assay Methodology: Quantitative Sandwich ELISA; ...
16. ALPRENOLOL [ԱԼՊՐԵՆՈԼՈԼ] 8. ALPHA-GALACTOSIDASES [ԱԼՖԱ-ԳԱԼԱԿՏՈԶԻԴԱԶՆԵՐ] 17. ALPROSTADIL [ԱԼՊՐՈՍՏԱԴԻԼ] 9. ALPHA-GLOBULINS [ ...
Alprenolol Action Pathway. smpdb. SMP00298. Atenolol Action Pathway. smpdb. SMP00299. Betaxolol Action Pathway. ...
Alprenolol * Glutathione / GST tag * Rho1D4 tag / 1D4 tag * StrepTactin * Activated Resins & MagBeads ...
1: X-ray crystal structure of ß2AR in complex with the antagonist alprenolol and the negative allosteric modulator.. To test ...
Morfolini: Fenbutrazat • Morazon • Fendimetrazin • Fenmetrazin; Oksazolini: 4-Metilaminoreks (4-MAR, 4-MAX) • Aminoreks • Klominoreks • Ciklazodon • Fenozolon • Fluminoreks • Pemolin • Tozalinon; Fenetilamini (takođe amfetamini, katinoni, fentermini, itd): 2-Hidroksifenetilamin (2-OH-PEA) • 4-CAB • 4-Metilamfetamin (4-MA) • 4-Metilmetamfetamin (4-MMA) • Alfetamin • Amfekloral • Amfepentoreks • Amfepramon • Amfetamin (Dekstroamfetamin • Levoamfetamin) • Amfetaminil • β-Metilfenetilamin (β-Me-PEA) • Benzodioksolilbutanamin (BDB) • Benzodioksolilhidroksibutanamin (BOH) • Benzfetamin • Bufedron • Butilon • Katin • Katinon • Klobenzoreks • Klortermin • D-deprenil • Dimetoksiamfetamin (DMA) • Dimetoksimetamfetamin (DMMA) • Dimetilamfetamin • Dimetilkatinon (Dimetilpropion, metamfepramon) • Etkatinon (Etilpropion) • Etilamfetamin • Etilbenzodioksolilbutanamin (EBDB) • Etilon • Famprofazon • Fenetilin • Fenproporeks ...
DOI för Gel formulations containing catanionic vesicles composed of alprenolol and SDS: effects of drug release and skin ... Gel formulations containing catanionic vesicles composed of alprenolol and SDS: effects of drug release and skin penetration on ...
ß-AR non-selective antagonists alprenolol and pindolol promoted ß-arrestin2 recruitment at ß1-AR. ß1-AR selective antagonists ...
Beta blockers (e.g., alprenolol, carteolol, cyanopindolol, iodocyanopindolol, isamoltane, oxprenolol, penbutolol, pindobind, ...
Antagonisti: Antipsihotici: Iloperidon • Risperidon • Sertindol; Beta blokatori: Alprenolol • Cianopindolol • Jodocianopindolol ...
Alprenolol *Alprostadil *Alprostadil Alfadex *Alsactide *Alseroxylon 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 ...
hydrochloride, alprenolol, NECA, CGS15943, endothelin-1 and. sulfisoxazole were from Tocris; LPA was obtained from Avanti Polar ...
Common nonselective beta blockers include alprenolol, carteolol, oxprenolol, propranolol and sotalol. As well as being used to ...
Reduced beta-adrenergic receptor concentrations in ageing man.
From the Alprenolol References models with the by applying Maya version 2018 Maya version 2018San ...
  • Alprenolol may increase the arrhythmogenic activities of Acebutolol. (drugbank.com)
  • Alprenolol has little to no intrinsic sympathomimetic activity and, unlike some other beta-adrenergic blocking agents, alprenolol has little direct myocardial depressant activity and does not have an anesthetic-like membrane-stabilizing action. (drugbank.com)
  • Alprenolol non-selectively blocks beta-1 adrenergic receptors mainly in the heart, inhibiting the effects of epinephrine and norepinephrine resulting in a decrease in heart rate and blood pressure. (drugbank.com)
  • complications ON CONGESTIVE HEART FAILURE Overview In this colitis, we will cause you a disease on Adrenergic patients suffering to risky failure Alprenolol. (worldclassbows.com)
  • One of the active metabolites, 4-OH-alprenolol, is an active beta-blocker. (drugbank.com)
  • The risk or severity of adverse effects can be increased when Alprenolol is combined with 1,2-Benzodiazepine. (drugbank.com)
  • Alprenolol hydrochloride is the hydrochloride salt form of alprenolol, which is an beta adrenergic receptor antagonist and is used as an antihypertensive, anti-anginal, and anti-arrhythmic agent. (selleckchem.com)
  • An incision was made in the skin Alprenolol hydrochloride overlying the skull and 0.3 ml ibotenic acid or phosphate-buffered saline (PBS) infused bilaterally into the ventral hippocampal formation (AP ?3.0 mm, ML 3.5 mm, VD ?5.0 mm relative to bregma) at a rate of 0.15 l/min. (seatra.org)
  • The needle was remaining in place for 1 min after infusion to Alprenolol hydrochloride facilitate diffusion. (seatra.org)
  • In rat, the Alprenolol hydrochloride ED50 for centrally acting serotonin 5-HT2 antagonism is definitely 14 g/kg (Megens et al, 1994), while the effects of D2 receptor antagonism 1st become apparent at 16 g/kg (Janssen et al, 1988), with an Alprenolol hydrochloride ED50 for D2 antagonism from 56 to 150 g/kg (Megens et al, 1994). (seatra.org)
  • They were attenuated by the mixed 5-HT1/5-HT2 receptor antagonist, methiotepin, the mixed 5-HT1A/5-HT1B receptor antagonist, (-)-alprenolol and the mixed 5-HT1A/5-HT2 receptor antagonist, spiperone, but not by the selective 5-HT1C/5-HT2 receptor antagonists, ritanserin, ICI 169,369 and ketanserin. (erowid.org)