Alprenolol
Sympatholytics
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.
Adrenergic beta-Antagonists
Pindolol
Practolol
Propranolol
Pentaerythritol Tetranitrate
Receptors, Adrenergic
Cell-surface proteins that bind epinephrine and/or norepinephrine with high affinity and trigger intracellular changes. The two major classes of adrenergic receptors, alpha and beta, were originally discriminated based on their cellular actions but now are distinguished by their relative affinity for characteristic synthetic ligands. Adrenergic receptors may also be classified according to the subtypes of G-proteins with which they bind; this scheme does not respect the alpha-beta distinction.
Receptors, Adrenergic, beta
Isoproterenol
Oxprenolol
Propanolamines
Dihydroalprenolol
Nadolol
Epinephrine
The active sympathomimetic hormone from the ADRENAL MEDULLA. It stimulates both the alpha- and beta- adrenergic systems, causes systemic VASOCONSTRICTION and gastrointestinal relaxation, stimulates the HEART, and dilates BRONCHI and cerebral vessels. It is used in ASTHMA and CARDIAC FAILURE and to delay absorption of local ANESTHETICS.
Pentobarbital
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)
Adrenergic beta-2 Receptor Antagonists
Anura
Receptors, Adrenergic, beta-2
A subclass of beta-adrenergic receptors (RECEPTORS, ADRENERGIC, BETA). The adrenergic beta-2 receptors are more sensitive to EPINEPHRINE than to NOREPINEPHRINE and have a high affinity for the agonist TERBUTALINE. They are widespread, with clinically important roles in SKELETAL MUSCLE; LIVER; and vascular, bronchial, gastrointestinal, and genitourinary SMOOTH MUSCLE.
Adenylate Cyclase
Respiratory Physiological Phenomena
Anesthesia, Intravenous
Norepinephrine
Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.
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)Electrophysiological effects of alprenolol on depressed canine myocardium<...
Alprenolol: Indication, Dosage, Side Effect, Precaution | MIMS Myanmar
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Alprenolol
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- ...
Alprenoxime
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 ...
Ralph Snyderman
... alprenolol binding". The Journal of Clinical Investigation. 57 (1): 149-155. doi:10.1172/JCI108254. PMC 436634. PMID 1245597. ...
Dihydroalprenolol
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. ...
List of drugs: Al
... alprenolol (INN) alprostadil (INN) alrestatin (INN) Alrex alsactide (INN) Altace (Pfizer/Sanofi-Aventis) Altamist altanserin ( ...
C15H23NO2
The molecular formula C15H23NO2 (molar mass : 249.34 g/mol) may refer to: Alprenolol Castoramine, an alkaloid found in ...
List of adrenergic drugs
Solabegron Terbutaline Tretoquinol Tulobuterol Xamoterol Zilpaterol Zinterol Acebutolol Adaprolol Adimolol Afurolol Alprenolol ...
Sympatholytic
Beta blockers Non-selective agents Alprenolol Bucindolol Carteolol Carvedilol (has additional α-blocking activity) Labetalol ( ...
5-HT1A receptor
ERK1/2 preferring agonist Alprenolol AV-965 Binospirone (postsynaptic 5-HT1A) BMY-7,378 Cannabigerol Cyanopindolol ...
List of MeSH codes (D02)
... 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 - ...
ATC code C07
C07AA01 Alprenolol C07AA02 Oxprenolol C07AA03 Pindolol C07AA05 Propranolol C07AA06 Timolol C07AA07 Sotalol C07AA12 Nadolol ...
C15H22N2O2
The molecular formula C15H22N2O2 may refer to: Alprenoxime, a beta blocker and prodrug to alprenolol Mepindolol, a non- ...
Alprenolol: Uses, Interactions, Mechanism of Action | DrugBank Online
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 ...
The Prohibited List | World Anti Doping Agency
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 ...
Chromolith RP-18e HighResolution HPLC Columns
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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 ...
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DeCS
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. ...
Code System Concept
Analyses
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 ...
Orphenadrine
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Acebutolol1
- Alprenolol may increase the arrhythmogenic activities of Acebutolol. (drugbank.com)
Adrenergic3
- 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)
Active1
- One of the active metabolites, 4-OH-alprenolol, is an active beta-blocker. (drugbank.com)
Effects1
- The risk or severity of adverse effects can be increased when Alprenolol is combined with 1,2-Benzodiazepine. (drugbank.com)
Hydrochloride4
- 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)
Antagonist1
- 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)