Alprenolol: One of the ADRENERGIC BETA-ANTAGONISTS used as an antihypertensive, anti-anginal, and anti-arrhythmic agent.Amino Alcohols: Compounds possessing both a hydroxyl (-OH) and an amino group (-NH2).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: 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.Pindolol: 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)Practolol: A beta-1 adrenergic antagonist that has been used in the emergency treatment of CARDIAC ARRYTHMIAS.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.Pentaerythritol Tetranitrate: A vasodilator with general properties similar to NITROGLYCERIN but with a more prolonged duration of action. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1025)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: 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.Isoproterenol: Isopropyl analog of EPINEPHRINE; beta-sympathomimetic that acts on the heart, bronchi, skeletal muscle, alimentary tract, etc. It is used mainly as bronchodilator and heart stimulant.Oxprenolol: A beta-adrenergic antagonist used in the treatment of hypertension, angina pectoris, arrhythmias, and anxiety.Adrenergic beta-Agonists: Drugs that selectively bind to and activate beta-adrenergic receptors.Propanolamines: AMINO ALCOHOLS containing the propanolamine (NH2CH2CHOHCH2) group and its derivatives.Dihydroalprenolol: 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.Nadolol: 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.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: Drugs that bind to and block the activation of ADRENERGIC BETA-2 RECEPTORS.Anura: 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.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: An enzyme of the lyase class that catalyzes the formation of CYCLIC AMP and pyrophosphate from ATP. EC 4.6.1.1.Respiratory Physiological Phenomena: Physiological processes and properties of the RESPIRATORY SYSTEM as a whole or of any of its parts.Anesthesia, Intravenous: Process of administering an anesthetic through injection directly into the bloodstream.Catecholamines: A general class of ortho-dihydroxyphenylalkylamines derived from tyrosine.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)... s, or glycosylceramides, are a class of lipids containing a backbone of sphingoid bases, a set of aliphatic amino alcohols that includes sphingosine. They were discovered in brain extracts in the 1870s and were named after the mythological Sphinx because of their enigmatic nature. These compounds play important roles in signal transmission and cell recognition. Sphingolipidoses, or disorders of sphingolipid metabolism, have particular impact on neural tissue. A sphingolipid with an R group consisting of a hydrogen atom only is a ceramide. Other common R groups include phosphocholine, yielding a sphingomyelin, and various sugar monomers or dimers, yielding cerebrosides and globosides, respectively. Cerebrosides and globosides are collectively known as glycosphingolipids. The long-chain bases, sometimes simply known as sphingoid bases, are the first non-transient products of de novo sphingolipid synthesis in both yeast and mammals. These compounds, specifically known as ...
In organic chemistry, mandelonitrile is the cyanohydrin derivative of benzaldehyde. Small amounts of mandelonitrile occur in the pits of some fruits. Mandelonitrile is the aglycone part of the cyanogenic glycosides prunasin and amygdalin. The naturally occurring (R)-(+) enantiomer finds use as an intermediate in the preparation of optically active α-hydroxy carboxylic acids, α-hydroxy aldehydes, α-hydroxy ketones, and 2-amino alcohols. Mandelonitrile can break down into cyanide and benzaldehyde, a reaction that can be catalyzed by the enzyme mandelonitrile lyase. Racemic mandelonitrile may be prepared similar to many other cyanohydrins. In a one pot reaction, benzaldehyde is reacted with sodium bisulfite to give the corresponding adduct, which further reacts with aqueous sodium cyanide to give the racemic product: Sigma-Aldrich product page The Merck Index (12th ed.). 1996. Kruse, C.G. In Collins, A.N. Sheldrake, G.N. Crosby, J., Eds. Chirality in Industry Chichester, UK , (1992), 279 Corson, ...
Ligands containing a chiral 2-oxazoline ring are used in asymmetric catalysis due to their facile synthesis, wide range of forms and effectiveness for many types of catalytic transformation.[23][24] 2-Substituted oxazolines can be prepared by many methods and possess a moderately hard N-donor. Chirality is easily incorporated by using 2-amino alcohols prepared by the reduction of amino acids; which are both optically pure and inexpensive. As the stereocentre in such oxazolines is adjacent to the coordinating N-atom, it can influence the selectivity of processes occurring at the metal centre. The ring is thermally stable[25] and resistant to nucleophiles, bases, radicals, and weak acids[26] as well as being fairly resistant to hydrolysis and oxidation;[7] thus it can be expected to remain stable in a wide range of reaction conditions. Major classes of oxazoline based ligand include: ...
... is the means by which a microbe obtains the energy and nutrients (e.g. carbon) it needs to live and reproduce. Microbes use many different types of metabolic strategies and species can often be differentiated from each other based on metabolic characteristics. The specific metabolic properties of a microbe are the major factors in determining that microbe's ecological niche, and often allow for that microbe to be useful in industrial processes or responsible for biogeochemical cycles. All microbial metabolisms can be arranged according to three principles: 1. How the organism obtains carbon for synthesising cell mass: autotrophic - carbon is obtained from carbon dioxide (CO2) heterotrophic - carbon is obtained from organic compounds mixotrophic - carbon is obtained from both organic compounds and by fixing carbon dioxide 2. How the organism obtains reducing equivalents used either in energy conservation or in biosynthetic reactions: lithotrophic - reducing equivalents are ...
A sympatholytic (or sympathoplegic) drug is a medication that opposes the downstream effects of postganglionic nerve firing in effector organs innervated by the sympathetic nervous system (SNS). They are indicated for various functions; for example, they may be used as antihypertensives. They are also used to treat anxiety, such as Generalized Anxiety Disorder, Panic Disorder and PTSD. Antiadrenergic agents inhibit the signals of epinephrine and norepinephrine. They are primarily postsynaptic adrenergic receptor antagonists (alpha and beta adrenergic receptor antagonists, or "blockers"), inhibiting the downstream cellular signaling pathways of adrenergic receptors. However, there are exceptions: clonidine is an adrenergic agonist at the α2 receptor; since this receptor is located presynaptically, agonism at this receptor inhibits the presynaptic release of adrenaline and noradrenaline, preventing postsynaptic adrenergic receptor activation and downstream signaling. Another way to inhibit ...
... (Etanor, Bronkephrine, Butanefrine) is a sympathomimetic and bronchodilator related to norepinephrine. It activates both α and β adrenergic receptors. Norepinephrine David J. Triggle (1996). Dictionary of Pharmacological Agents. Boca Raton: Chapman & Hall/CRC. ISBN 0-412-46630-9. KORNEL L (1958). "A case of calcified ventricular aneurysm with progressive heart block; observations on the effect of ethylnorepinephrine". Cardiologia. 32 (2): 101-9. doi:10.1159/000165806. PMID 13500349. CHRISTENSEN JM, VALASEK FE, TAINTER ML (June 1958). "Ethylnorepinephrine; a unique bronchodilator". American Practitioner and Digest of Treatment. 9 (6): 916-21. PMID 13533786. Turner, Robert A. (1965). "12. Sympatholytic Agents. VI. The Two Kinds of Receptors". Screening Methods in Pharmacology. 111 Fifth Avenue, New York, New York 10003: Academic Press Inc. p. 150. ISBN 1483255913 ...
... (brand names Trasacor, Trasicor, Coretal, Laracor, Slow-Pren, Captol, Corbeton, Slow-Trasicor, Tevacor, Trasitensin, Trasidex) is a non-selective beta blocker with some intrinsic sympathomimetic activity. It is used for the treatment of angina pectoris, abnormal heart rhythms and high blood pressure. Oxprenolol is a lipophilic beta blocker which passes the blood-brain barrier more easily than water-soluble beta blockers. As such, it is associated with a higher incidence of CNS-related side effects than hydrophilic ligands such as atenolol, sotalol and nadolol. Oxprenolol is a potent beta blocker and should not be administered to asthmatics under any circumstances due to their low beta levels as a result of depletion due to other asthma medication, and because it can cause irreversible, often fatal, airway failure and inflammation. Oxprenolol is a beta blocker. In addition, it has been found to act as an antagonist of the serotonin 5-HT1A and 5-HT1B receptors with respective Ki values ...
Adverse drug reactions associated with the use of beta blockers include: nausea, diarrhea, bronchospasm, dyspnea, cold extremities, exacerbation of Raynaud's syndrome, bradycardia, hypotension, heart failure, heart block, fatigue, dizziness, alopecia (hair loss), abnormal vision, hallucinations, insomnia, nightmares, sexual dysfunction, erectile dysfunction and/or alteration of glucose and lipid metabolism. Mixed α1/β-antagonist therapy is also commonly associated with orthostatic hypotension. Carvedilol therapy is commonly associated with edema.[44] Due to the high penetration across the blood-brain barrier, lipophilic beta blockers, such as propranolol and metoprolol, are more likely than other less lipophilic beta blockers to cause sleep disturbances, such as insomnia, vivid dreams and nightmares.[45]. Adverse effects associated with β2-adrenergic receptor antagonist activity (bronchospasm, peripheral vasoconstriction, alteration of glucose and lipid metabolism) are less common with ...
Adverse drug reactions associated with the use of beta blockers include: nausea, diarrhea, bronchospasm, dyspnea, cold extremities, exacerbation of Raynaud's syndrome, bradycardia, hypotension, heart failure, heart block, fatigue, dizziness, alopecia (hair loss), abnormal vision, hallucinations, insomnia, nightmares, sexual dysfunction, erectile dysfunction and/or alteration of glucose and lipid metabolism. Mixed α1/β-antagonist therapy is also commonly associated with orthostatic hypotension. Carvedilol therapy is commonly associated with edema.[44] Due to the high penetration across the blood-brain barrier, lipophilic beta blockers, such as propranolol and metoprolol, are more likely than other less lipophilic beta blockers to cause sleep disturbances, such as insomnia, vivid dreams and nightmares.[45] Adverse effects associated with β2-adrenergic receptor antagonist activity (bronchospasm, peripheral vasoconstriction, alteration of glucose and lipid metabolism) are less common with ...
... se upotrebljava za liječenje hipertenzije i za dugotrajni tretman angine pectoris, a američka agencija FDA ga je odobrila za ove svrhe.[2] Regularno se koristi povremeno[2]za praćenje otkucaja srca u osoba sa fibrilacijom atrija,[3] prevenciju migrenskih glavobolja,[4] i krvarenja vena kod osoba sa portnom hipertenzijom koju uzrokuje ciroza;[5] za liječenje visokog nivoa hormona štitnjače.[6] Nadolol je jedan od preferiranih beta blokatora u upravljanju bolesnicima sa LQTS, za skraćenje QT intervala i prevenciju ventrikulske aritmije. U prevenciji srčanih tegoba, efikasniji je od metoprolola, dok na napredak terapije je jednak propranololu.[7] Nadolol ima prednost za jednodnevno doziranje i poboljšavanje usklađenosti pacijenta. Kod pacijenata sa smanjenom funkcijom bubrega, nadolol se može rjeđe dozirati.[8]Također je upotrebljiv za propisivanje lijeka za drugo stanje od onog za koje je zvanično odobreno za nekoliko nervnih poremećaja, kao što su prevencija napada ...
InChI=1S/C23H28N2O3/c1-16-13-19-20(25-16)11-8-12-21(19)27-15-18(14-24-23(2,3)4)28-22(26)17-9-6-5-7-10-17/h5-13,18,24-25H,14-15H2,1- ...
InChI=1S/C20H27NO4/c1-15-5-4-6-18(11-15)25-14-17(22)13-21-10-9-16-7-8-19(23-2)20(12-16)24-3/h4-8,11-12,17,21-22H,9-10,13-14H2,1-3H3 ...
ନାଡୋଲୋଲ (ଇଂରାଜୀ ଭାଷାରେ Nadolol) ଏକ ବିକ୍ରୟ ନାମ କୋରଗାର୍ଡ଼/ Corgard) ଏକ ଔଷଧ ଯାହା ଉଚ୍ଚ ରକ୍ତଚାପ, ଆଞ୍ଜାଇନା ପେକ୍ଟୋରିସ (heart pain) ଓ ଆଟ୍ରିଆଲ ଫିବ୍ରିଲେସନ ରୋଗମାନଙ୍କର ଚିକିତ୍ସାରେ ଦିଆଯାଏ ।[୧] ପ୍ରତିଷେଧକ ଭାବରେ ଅଧକପାଳି ଓ ସିରୋସିସ୍ ରୋଗରେ ଦିଆଯାଏ ।[୨][୩] ଏହି ଔଷଧ ପାଟିରେ ଦିଆଯାଏ । [୨] ନାଡୋଲୋଲର ପାର୍ଶ୍ୱ ପ୍ରତିକ୍ରିୟାରେ ମୁଣ୍ଡ ଓଜନିଆ, ଥକ୍କା ଅନୁଭବ, ଧୀର ହୃଦ୍ଗତି (slow heart rate) ଓ ରେନଡ ସିଣ୍ଡ୍ରୋମ ଇତ୍ୟାଦି ହୋଇପାରେ ।[୧] ପାର୍ଶ୍ୱ ପ୍ରତିକ୍ରିୟା ...