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Alpha Adrenergic Antagonist

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81. Ectopic beta-adrenergic receptor binding sites. possible molecular basis of aberrant catecholamine responsiveness of an adrenocortical tumor adenylate cyclase. (PubMed)

] dihydroalprenolol with an equilibrium dissociation constant of 2.1 nM. Adrenergic agonists competed for the binding sites in an order of potency, [(-) isoproterenol greater than (-) epinephrine (-) norepinephrine], paralleling their order of potency as beta-adrenergic agonists. The beta-adrenergic antagonist, (-) propranolol, competed for binding, causing half-mzximal inhibition of specific binding at a concentration of 6 nM. The alpha-adrenergic antagonist, phentolamine, and several catecholamine metabolites (...) and precursors did not effectively compete for the binding sites at high concentrations. Binding was stereospecific, the (+) stereoisomers of beta-adrenergic agonists and antagonists requiring 40- to 300-fold higher concentrations than the corresponding (-) stereoisomers to half maximally inhibit (-) [3H] dihydroalprenolol binding. These results indicate that adrenocortical carcinoma 494 membranes contain beta-adrenergic receptor-binding sites which are not normally present in membranes of adrenal tissue

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1977 Journal of Clinical Investigation

82. The effects of labetalol (AH 5158) on adrenergic transmission in the cat spleen. (PubMed)

The effects of labetalol (AH 5158) on adrenergic transmission in the cat spleen. 1. The competitive alpha- and beta-adrenoceptor blocking agent labetalol, in concentrations up to 10(-4) M, produced dose-dependent increases in transmitter overflow from the isolated blood perfused spleen of the cat following nerve stimulation at 10 and 30 Hz. 2. At concentrations above 10(-4) M labetol produced a pronounced decrease in transmitter overflow. 3. Labetalol (1.5 X 10(-4) M) increased the recovery (...) antagonist in the isolated blood perfused spleen of the cat with little effect on presynaptic alpha-adrenoceptors. The moderate elevation of transmitter overflow by the drug is related to the inhibitory effect of the drug on neuronal uptake rather than on presynaptic alpha-adrenoceptors.

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1977 British journal of pharmacology

83. Characterization of the Human Platelet α-Adrenergic Receptor: CORRELATION OF [3H] DIHYDROERGOCRYPTINE BINDING WITH AGGREGATION AND ADENYLATE CYCLASE INHIBITION (PubMed)

Characterization of the Human Platelet α-Adrenergic Receptor: CORRELATION OF [3H] DIHYDROERGOCRYPTINE BINDING WITH AGGREGATION AND ADENYLATE CYCLASE INHIBITION Human platelets aggregate and undergo a release reaction when incubated with catecholamines. Indirect evidence indicates that these events are mediated through alpha-adrenergic receptors. We used [(3)H]dihydroergocryptine, an alpha-adrenergic antagonist, to identify binding sites on platelets that have the characteristics of alpha (...) platelet. The K(d) for [(3)H]-dihydroergocryptine was 0.003-0.01 muM. The alpha-adrenergic antagonist phentolamine (K(d) = 0.0069 muM) was much more potent than the beta-adrenergic antagonist (+/-) propranolol (K(d) = 27 muM) in competing for the binding sites. The binding data were correlated with catecholamine-induced platelet aggregation and inhibition of basal and prostaglandin E(1)-stimulated adenylate cyclase. (-) Epinephrine was more potent than (-) norepinephrine in producing aggregation

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1978 Journal of Clinical Investigation

84. Selective labeling of α-adrenergic receptors in caudate nucleus by [3H]dihydroergocryptine in the presence of spiperone-blocked dopamine receptors (PubMed)

) was revealing alpha receptors. The alpha-adrenergic antagonists also competed for binding in the appropriate order: phentolamine > phenoxybenzamine > dibenamine. Finally, chlorpromazine was more potent than haloperidol in competing for [(3)H]dihydroergocryptine, also in accord with the properties of alpha receptors. These results with [(3)H]dihydroergocryptine as an alpha-adrenergic receptor ligand correlate well with those published by others for [(3)H]WB-4101. (...) Selective labeling of α-adrenergic receptors in caudate nucleus by [3H]dihydroergocryptine in the presence of spiperone-blocked dopamine receptors Because it was known that [(3)H]dihydroergocryptine can label alpha-adrenergic receptors as well as dopamine receptors, this study was done to establish the conditions under which [(3)H]dihydroergocryptine would be a reliable ligand for selective labeling of alpha-adrenergic receptors. The calf caudate was chosen because it contains both dopamine

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1978 Proceedings of the National Academy of Sciences of the United States of America

85. Initial investigations into adrenaline accumulation and adrenergic responsiveness in cultured neonatal rat heart cells. (PubMed)

-concentration data were not linearly correlated with dose-response data. 4 Accumulation did not correlate well with beta-adrenoceptor responsiveness in a number of situations of varying responsiveness. 5 Accumulation was not blocked by a variety of uptake blocking agents or alpha- and beta-adrenoceptor antagonists. 6 A much smaller accumulation process was observed in fibroblasts which respond to adrenaline with reversible morphological changes. (...) Initial investigations into adrenaline accumulation and adrenergic responsiveness in cultured neonatal rat heart cells. 1 Accumulation of tritiated adrenaline (and/or its products) has been studied by a variety of techniques in viable, attached and free-floating myoblasts cultured from neonatal rat heart cells. 2 Accumulation increased with the number of cells used, the culture age of cells, incubation time and the concentration of adrenaline in the incubation mixture. 3 Accumulation

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1978 British journal of pharmacology

86. Identification of α-Adrenergic Receptors in Human Platelets by [3H]Dihydroergocryptine Binding (PubMed)

potent than the (-)isomers. The potent alpha-adrenergic antagonists phentolamine, phenoxybenzamine, and yohimbine competed potently for the sites, whereas beta-antagonists such as propranolol and dichlorisoproterenol were quite weak. Dopamine and serotonin competed only at high concentrations (0.1 mM). The [(3)H]dihydroergocryptine binding sites could also be demonstrated in intact platelets where they displayed comparable specificity, stereospecificity, and saturability. Saturation binding studies (...) with the intact platelets indicated 220+/-45 receptors per platelet, in good agreement with the value derived from studies with platelet lysates. Ability of alpha-adrenergic agonists to inhibit adenylate cyclase and of alpha-adrenergic antagonists to antagonize this inhibitory effect directly paralleled ability to interact with the [(3)H]dihydroergocryptine binding sites. These data demonstrate the feasibility of directly studying alpha-adrenergic receptor binding sites in human platelets with [(3)H

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1978 Journal of Clinical Investigation

87. Pulmonary Alveolar Type II Cells Isolated from Rats: RELEASE OF PHOSPHATIDYLCHOLINE IN RESPONSE TO β-ADRENERGIC STIMULATION (PubMed)

phosphatidylcholine in 3 h; the concentration of terbutaline causing half maximal stimulation was 800 nM. The terbutaline effect was blocked by propranolol, a beta-adrenergic antagonist (calculated K(d) = 6 nM), but not by phentolamine, an alpha-adrenergic antagonist. Isobutylmethylxanthine, a phosphodiesterase inhibitor, and 8-Br cyclic AMP, but not 8-Br cyclic guanosine monophosphate, also stimulated release. We conclude that type II cells secrete disaturated phosphatidylcholine in response to treatment (...) Pulmonary Alveolar Type II Cells Isolated from Rats: RELEASE OF PHOSPHATIDYLCHOLINE IN RESPONSE TO β-ADRENERGIC STIMULATION It is unclear what factors control the secretion of pulmonary surface active material from alveolar type II cells in vivo. Other workers have suggested that cholinergic stimuli, adrenergic stimuli, and prostaglandins may all stimulate secretion. We isolated type II cells from the lungs of rats by treatment with elastase, discontinuous density centrifugation, and adherence

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1979 Journal of Clinical Investigation

88. Beta-Adrenergic Potentiation of the Increased In Vitro Accumulation of Cycloleucine by Rat Thymocytes Induced by Triiodothyronine (PubMed)

by the concomitant addition of epinephrine, norepinephrine, and possibly isoproterenol, whereas terbutaline and phenylephrine were without effect. Neither basal nor T(3)-enhanced CLE accumulation was affected by the addition alone of the adrenergic blocking agents, propranolol (0.1 mM), phentolamine (10 muM), or practolol (0.1 mM). Nevertheless, the beta(1)- and beta(2)-antagonist, propranol, and the beta(1)-antagonist, practolol, blocked the increment in CLE accumulation produced by epinephrine; the alpha (...) Beta-Adrenergic Potentiation of the Increased In Vitro Accumulation of Cycloleucine by Rat Thymocytes Induced by Triiodothyronine We have previously demonstrated that 3,5,3'-triiodothyronine (T(3)), whether administered in vivo or added to suspending media in vitro, promptly stimulates the in vitro accumulation of the nonmetabolized amino acids, alpha-aminoisobutyric acid, and cycloleucine (CLE) by thymocytes isolated from weanling rats. In these studies, we have examined the in vitro

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1979 Journal of Clinical Investigation

89. The nature of the adrenergic receptors in isolated human bronchi (PubMed)

The nature of the adrenergic receptors in isolated human bronchi 4390657 1969 12 18 2018 11 13 0040-6376 24 5 1969 Sep Thorax Thorax The nature of the adrenergic receptors in isolated human bronchi. 613-5 Guirgis H M HM McNeill R S RS eng Journal Article England Thorax 0417353 0040-6376 0 Adrenergic alpha-Antagonists 0 Adrenergic beta-Antagonists 0 Receptors, Drug 0TTZ664R7Z Phenoxybenzamine 820484N8I3 Histamine 8Y164V895Y Carbachol 9Y8NXQ24VQ Propranolol N9YNS0M02X Acetylcholine YKH834O4BH (...) Epinephrine Z468598HBV Phentolamine IM Acetylcholine pharmacology Adrenergic alpha-Antagonists pharmacology Adrenergic beta-Antagonists pharmacology Bronchi drug effects Carbachol pharmacology Drug Synergism Epinephrine antagonists & inhibitors pharmacology Histamine pharmacology Humans In Vitro Techniques Muscle Contraction drug effects Phenoxybenzamine pharmacology Phentolamine pharmacology Propranolol pharmacology Receptors, Drug 1969 9 1 1969 9 1 0 1 1969 9 1 0 0 ppublish 4390657 PMC472060 Int Arch

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1969 Thorax

90. Adrenergic receptors in human veins. (PubMed)

Adrenergic receptors in human veins. 4392768 1970 07 06 2018 11 13 0008-4409 102 12 1970 Jun 06 Canadian Medical Association journal Can Med Assoc J Adrenergic receptors in human veins. 1297-9 Beck J R JR Nadasdi M M Zsotér T T TT eng Journal Article Canada Can Med Assoc J 0414110 0008-4409 0 Adrenergic alpha-Antagonists 0 Adrenergic beta-Antagonists 9Y8NXQ24VQ Propranolol L628TT009W Isoproterenol X4W3ENH1CV Norepinephrine Z468598HBV Phentolamine AIM IM Adrenergic alpha-Antagonists Adrenergic (...) beta-Antagonists Adult Aged Female Humans Isoproterenol Male Norepinephrine Phentolamine Propranolol Sensory Receptor Cells physiology Vasomotor System physiology Veins innervation Venous Pressure 1970 6 6 1970 6 6 0 1 1970 6 6 0 0 ppublish 4392768 PMC1930261 Am J Physiol. 1965 Aug;209:383-9 14321138 J Pharmacol Exp Ther. 1964 May;144:156-62 14183426 J Clin Invest. 1959 Feb;38(2):342-6 13631065 Eur J Pharmacol. 1969 Jan;5(2):133-40 4389638 Med Clin North Am. 1968 Sep;52(5):1009-16 4876824 Br J

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1970 Canadian Medical Association Journal

91. Vagal non-adrenergic inhibition of guinea-pig stomach (PubMed)

Vagal non-adrenergic inhibition of guinea-pig stomach 1. The effect of vagal and sympathetic stimulation on the mechanical and electrical activity (intracellular recording) of the body of the guinea-pig stomach was investigated in vitro.2. Following atropine, 1 x 10(-6)-1 x 10(-7) g/ml., vagal responses were reversed from excitatory to inhibitory.3. Sympathetic blockade, produced by alpha- and beta-receptor antagonists and adrenergic neurone-blocking agents, reduced or abolished sympathetic (...) of the inhibitory non-adrenergic transmitter, released by the intramural neurones activated by preganglionic vagal fibres, is discussed.

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1971 The Journal of physiology

92. Responses of coronary vessels to adrenergic stimuli (PubMed)

responses to isoproterenol in the paw were not altered by practolol. Practolol antagonized the increases in dp/dt, heart rate, and systolic pressure and reversed coronary responses to norepinephrine and nerve stimulation from dilatation to constriction. The constriction, in turn, was reduced or reversed by phentolamine, an alpha receptor antagonist. Propranolol did not augment the constriction seen in response to norepinephrine and nerve stimulation after practolol. These results indicate (...) Responses of coronary vessels to adrenergic stimuli Coronary responses to adrenergic stimuli were determined in the intact beating heart before and after administration of practolol, 4-(2-hydroxy-3-isopropylaminoproproxy) acetanilide, which in low doses blocks myocardial but not vascular beta receptors. The left circumflex coronary artery of dogs was perfused with arterial blood at constant flow, and coronary perfusion pressure was measured. Before practolol, intracoronary injections

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1971 Journal of Clinical Investigation

93. Central cholinergic and adrenergic mechanisms in the release of antidiuretic hormone (PubMed)

Central cholinergic and adrenergic mechanisms in the release of antidiuretic hormone 1. Studies on the urine outflow, blood ADH concentration and electrolyte excretion were carried out in alpha-chloralose anaesthetized hydrated dogs; the agonists and antagonists of specific cholinoceptors and adrenoceptors were injected by the intracerebroventricular technique, to delineate the role of the C.N.S. receptors in the control of ADH secretion.2. Central injection of acetylcholine elicited a dose (...) -dependent antidiuretic response which was associated with an increase in the blood ADH titre. Central atropinization partially blocked the antidiuretic response. The remaining antidiuretic response was reversed to a diuretic one by further pretreatment with phenoxybenzamine. The diuretic response thus obtained could be blocked by propranolol.3. The alpha-adrenoceptor agonists, phenylephrine and noradrenaline, induced dose-dependent antidiuretic responses with a concomitant rise in blood ADH

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1972 British journal of pharmacology

94. Effect of renal nerve stimulation, renal blood flow and adrenergic blockade on plasma renin activity in the cat (PubMed)

gradually returned to control values over approximately the next 10 min in spite of continued stimulation for up to 30 min.2. Plasma renin activity (PRA) increased markedly after 10 min of stimulation but 20 min later fell towards pre-stimulation values whether stimulation was maintained or not.3. Phentolamine, an alpha-adrenergic-receptor antagonist, abolished both the blood flow and PRA responses to a 10 min period of renal nerve stimulation.4. When the renal artery was constricted in order to produce (...) blood flow changes similar to those found with renal nerve stimulation, the rise in PRA was similar to that observed with renal stimulation.5. In phentolamine-blocked animals, renal artery constriction, as described, produced the same effect on PRA as was observed with renal nerve stimulation.6. Propranolol, a beta-adrenergic-receptor antagonist, did not block the blood flow response to renal nerve stimulation, but did block the rise in PRA normally associated with renal nerve stimulation.7

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1972 The Journal of physiology

95. The Adrenergic Control of Lower Esophageal Sphincter Function: AN EXPERIMENTAL MODEL OF DENERVATION SUPERSENSITIVITY (PubMed)

The Adrenergic Control of Lower Esophageal Sphincter Function: AN EXPERIMENTAL MODEL OF DENERVATION SUPERSENSITIVITY To evaluate the adrenergic regulation of lower esophageal sphincter (LES) function, LES pressure, LES relaxation during swallowing, and blood pressure were measured in the anesthetized opossum, Didelphis virginiana, during intravenous administration of alpha and beta adrenergic agonists and antagonists. Studies were done in controls and animals adrenergically denervated with 6 (...) -hydroxydopamine. Alpha adrenergic agonists (norepinephrine, phenylephrine) increased LES pressure and blood pressure, whereas a beta adrenergic agonist (isoproterenol) decreased both pressures. Alpha adrenergic antagonism (phentolamine) reduced basal LES pressure by 38.3+/-3.8% (mean +/-SEM) (P < 0.001). Beta adrenergic antagonism (propranolol) had no significant effect on either basal LES pressure or percent of LES relaxation with swallowing. After adrenergic denervation with 6-hydroxydopamine, basal LES

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1973 Journal of Clinical Investigation

96. Adrenergic Modulation of Pancreatic Glucagon Secretion in Man (PubMed)

Adrenergic Modulation of Pancreatic Glucagon Secretion in Man In order to characterize the influence of the adrenergic system on pancreatic glucagon secretion in man, changes in basal glucagon secretion during infusions of pure alpha and beta adrenergic agonists and their specific antagonists were studied. During infusion of isoproterenol (3 mug/min), a beta adrenergic agonist, plasma glucagon rose from a mean (+/-SE) basal level of 104+/-10 to 171+/-15 pg/ml, P < 0.0002. Concomitant infusion (...) of propranolol (80 mug/min), a beta adrenergic antagonist, prevented the effects of isoproterenol, although propranolol itself had no effect on basal glucagon secretion. During infusion of methoxamine (0.5 mg/min), an alpha adrenergic agonist, plasma glucagon declined from a mean basal level of 122+/-15 to 75+/-17 pg/ml, P < 0.001. Infusion of phentolamine (0.5 mg/min), an alpha adrenergic antagonist, caused a rise in plasma glucagon from a mean basal level of 118+/-16 to 175+/-21 pg/ml, P < 0.0001

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1974 Journal of Clinical Investigation

97. Costs and persistence of carbonic anhydrase inhibitor versus alpha-2 agonists, associated with beta-blockers, in glaucoma and ocular hypertension: an analysis of the UK-GPRD database

MeSH Adrenergic alpha-Agonists /administration & Adrenergic beta-Antagonists /administration & Aged; Carbonic Anhydrase Inhibitors /administration & Cohort Studies; Confidence Intervals; Cost of Illness; Cost-Benefit Analysis; Dose-Response Relationship, Drug; Drug Administration Schedule; Drug Therapy, Combination; Female; Glaucoma /diagnosis /drug therapy; Great Britain; Humans; Intraocular Pressure /drug effects; Male; Middle Aged; Ocular Hypertension /diagnosis /drug therapy; Probability (...) hypertension: an analysis of the UK-GPRD database Lafuma A, Berdeaux G Record Status This is a critical abstract of an economic evaluation that meets the criteria for inclusion on NHS EED. Each abstract contains a brief summary of the methods, the results and conclusions followed by a detailed critical assessment on the reliability of the study and the conclusions drawn. CRD summary This study compared the clinical and economic impact of alpha-2 adrenergic agonists and carbonic anhydrase inhibitors (CAIs

2008 NHS Economic Evaluation Database.

98. Cost-effectiveness of medical expulsive therapy using alpha-blockers for the treatment of distal ureteral stones

. Lancet 2006; 368: 1171-1179. Chandhoke PS. When is medical prophylaxis cost-effective for recurrent calcium stones? Journal of Urology 2002; 168: 937-940. Indexing Status Subject indexing assigned by NLM MeSH Adrenergic alpha-Antagonists /economics /therapeutic use; Cost-Benefit Analysis; Female; Germany /epidemiology; Great Britain /epidemiology; Humans; Incidence; Italy /epidemiology; Male; Observation; Sulfonamides /economics /therapeutic use; Turkey /epidemiology; United States /epidemiology (...) alone, even when the success rate with tamsulosin was only marginally superior to that with observation. CRD commentary Interventions: The indication, dose, and frequency of the tamsulosin were well described, but it was not clear why calcium-channel blockers and alpha-receptor antagonists were not evaluated. Medical expulsive therapy might not be feasible in some settings, for instance, alpha-blockers were not approved for the treatment of ureteral stones in the USA. Effectiveness/benefits

2008 NHS Economic Evaluation Database.

99. Alpha-Blockers in Allergic Rhinitis (MAN 01)

Infections Otorhinolaryngologic Diseases Respiratory Hypersensitivity Hypersensitivity, Immediate Hypersensitivity Immune System Diseases Doxazosin Antihypertensive Agents Adrenergic alpha-1 Receptor Antagonists Adrenergic alpha-Antagonists Adrenergic Antagonists Adrenergic Agents Neurotransmitter Agents Molecular Mechanisms of Pharmacological Action Physiological Effects of Drugs (...) or decreased lumen diameter of the gastrointestinal tract. Concomitant use of PDE5 inhibitors (sildenafil etc.) Alpha antagonists - this is the medication under investigation. Other cardiovascular medications including but not limited to: ACE inhibitors, Angiotensin II antagonists, Beta blockers, calcium channel blockers, diuretics, nitrates, phosphodiesterase type-5 inhibitors or other vasodilating medications - these in combination with doxazosin carry an increased risk of symptomatic hypotension

2013 Clinical Trials

100. Hemodynamic Response of Neuropathic And Non-Neuropathic POTS Patients To Adrenoreceptor Agonist And Antagonist

: No Criteria Inclusion Criteria: CDC criteria for chronic fatigue syndrome Evidence of postural tachycardia syndrome with symptoms of orthostatic intolerance Exclusion Criteria: Pregnant or lactating females. The administration of droxidopa is harmful to the fetus Concomitant therapy with anticholinergic, alpha-, and beta-adrenergic antagonists or other medications that affect autonomic function Clinically significant coronary artery, cerebrovascular or peripheral vascular disease Cardiac arrhythmias (...) will have different responsiveness than patients with neuropathic POTS to direct alpha-1 adrenoreceptor agonist therapy (droxidopa) and to non-selective beta-adrenoreceptor antagonist therapy (atenolol). The specific goal of this protocol is to investigate the effect of atenolol and droxidopa on cardiovascular autonomic functions such as cardiovagal control, sympathetic nerve activity, and sympathetic vascular transduction, systemic hemodynamic response to orthostatic stress and on the quality of life

2012 Clinical Trials

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