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Alpha Adrenergic Antagonist

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61. Combining benefits of an adrenergic and a muscarinic blocker in a single formulation - a pharmacokinetic evaluation. (Abstract)

Combining benefits of an adrenergic and a muscarinic blocker in a single formulation - a pharmacokinetic evaluation. A pharmacokinetic bioequivalence study was conducted in Asian subjects, to compare a fixed dose combination capsule single oral dose of alpha adrenoceptor blocker-Alfuzosin hydrochloride 10mg extended release and muscarinic antagonists-Solifenacin succinate 5mg against individually administered Xatral XL 10mg tablets (Alfuzosin) of Sanofi Synthelabo Limited, United Kingdom (UK

2013 Regulatory toxicology and pharmacology : RTP Controlled trial quality: uncertain

62. Beta Adrenergic Receptor

. Related Studies (from Trip Database) Ontology: Receptors, Adrenergic, beta-1 (C0001642) Definition (MSH) A subclass of beta-adrenergic receptors (RECEPTORS, ADRENERGIC, BETA). The adrenergic beta-1 receptors are equally sensitive to EPINEPHRINE and NOREPINEPHRINE and bind the agonist DOBUTAMINE and the antagonist METOPROLOL with high affinity. They are found in the HEART, juxtaglomerular cells, and in the central and peripheral nervous systems. Definition (NCI) Beta 1 adrenergic receptor protein (477 (...) adrenergic fibers, Beta Adrenergic Receptors are one of two major classes of adrenergic receptors (alpha and beta) based on their reactions to norepinephrine and epinephrine, on cellular effects of receptor activation, and on relative affinities and reactions to synthetic blocking or stimulating agents. Beta-adrenergic receptors respond to blocking agents such as propranolol and to activating agents such as isoproterenol. Beta-1 type receptors mediate lipolysis and increase cardiac rate and force

2015 FP Notebook

63. Treatment of Schizophrenia With L-tetrahydropalmatine (l-THP): a Novel Dopamine Antagonist With Anti-inflammatory and Antiprotozoal Activity

Treatment of Schizophrenia With L-tetrahydropalmatine (l-THP): a Novel Dopamine Antagonist With Anti-inflammatory and Antiprotozoal Activity Treatment of Schizophrenia With L-tetrahydropalmatine (l-THP): a Novel Dopamine Antagonist With Anti-inflammatory and Antiprotozoal Activity - Full Text View - ClinicalTrials.gov Hide glossary Glossary Study record managers: refer to the if submitting registration or results information. Search for terms x × Study Record Detail Saved Studies Save (...) this study Warning You have reached the maximum number of saved studies (100). Please remove one or more studies before adding more. Treatment of Schizophrenia With L-tetrahydropalmatine (l-THP): a Novel Dopamine Antagonist With Anti-inflammatory and Antiprotozoal Activity The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. of clinical studies and talk to your

2014 Clinical Trials

64. Study to Assess the Influence of Three Different α-antagonists and Placebo on the Extent of Weekly Phenylephrine-induced Mydriasis at Three Different Concentrations of Phenylephrine in Healthy Male Volunteers

Agents Adrenergic alpha-1 Receptor Antagonists Adrenergic alpha-Antagonists Adrenergic Antagonists Urological Agents Antihypertensive Agents (...) table for MeSH terms Mydriasis Pupil Disorders Eye Diseases Phenylephrine Oxymetazoline Tamsulosin Doxazosin Alfuzosin Cardiotonic Agents Mydriatics Autonomic Agents Peripheral Nervous System Agents Physiological Effects of Drugs Sympathomimetics Vasoconstrictor Agents Nasal Decongestants Respiratory System Agents Adrenergic alpha-1 Receptor Agonists Adrenergic alpha-Agonists Adrenergic Agonists Adrenergic Agents Neurotransmitter Agents Molecular Mechanisms of Pharmacological Action Protective

2014 Clinical Trials

65. Identification of cardiac beta-adrenergic receptors by (minus) [3H]alprenolol binding. Full Text available with Trip Pro

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

1975 Proceedings of the National Academy of Sciences of the United States of America

66. Adrenergic Modulation of Pancreatic Glucagon Secretion in Man Full Text available with Trip Pro

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

1974 Journal of Clinical Investigation

67. Proceedings: Adrenergic blockade and the pulmonary pressor response to lactic acid. Full Text available with Trip Pro

Proceedings: Adrenergic blockade and the pulmonary pressor response to lactic acid. 238708 1975 10 30 2018 11 13 0007-1188 54 2 1975 Jun British journal of pharmacology Br. J. Pharmacol. Proceedings: Adrenergic blockade and the pulmonary pressor response to lactic acid. 262P James W R WR Thomas A J AJ eng Journal Article England Br J Pharmacol 7502536 0007-1188 0 Adrenergic alpha-Antagonists 0 Adrenergic beta-Antagonists 0 Lactates IM Adrenergic alpha-Antagonists pharmacology Adrenergic beta (...) -Antagonists pharmacology Animals Blood Pressure drug effects Drug Interactions Lactates antagonists & inhibitors pharmacology Pulmonary Circulation drug effects Sheep 1975 6 1 1975 6 1 0 1 1975 6 1 0 0 ppublish 238708 PMC1666597 Q J Exp Physiol Cogn Med Sci. 1969 Apr;54(2):156-72 5193730 J Clin Invest. 1971 May;50(5):1028-43 5552405

1975 British journal of pharmacology

68. Immunological release of histamine from bovine leucocytes. Unusual adrenergic modulation. Full Text available with Trip Pro

Immunological release of histamine from bovine leucocytes. Unusual adrenergic modulation. Sensitized bovine granulocytes release histamine when exposed to specific antigen. In comparison with in vitro systems in several other species, the modulation of this release by adrenergic agents is unique. Beta-Adrenoceptor stimulation potentiates (rather than inhibits), whereas alpha-adrenoceptor stimulation inhibits (rather than potentiates) histamine release. Adrenaline, which is generally considered (...) to be a physiological antagonist of the anaphylactic reaction, potentiated histamine release in this study. Dopamine, which is present in high concentration in bovine mast cells, was without effect. The results are discussed in terms of the possible role of granulocytes in bovine hypersensitivity.

1976 Immunology

69. Central cholinergic and adrenergic mechanisms in the release of antidiuretic hormone Full Text available with Trip Pro

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

1972 British journal of pharmacology

70. The nature of the adrenergic receptors in isolated human bronchi Full Text available with Trip Pro

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

1969 Thorax

71. Vagal non-adrenergic inhibition of guinea-pig stomach Full Text available with Trip Pro

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.

1971 The Journal of physiology

72. Effect of renal nerve stimulation, renal blood flow and adrenergic blockade on plasma renin activity in the cat Full Text available with Trip Pro

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

1972 The Journal of physiology

73. The Adrenergic Control of Lower Esophageal Sphincter Function: AN EXPERIMENTAL MODEL OF DENERVATION SUPERSENSITIVITY Full Text available with Trip Pro

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

1973 Journal of Clinical Investigation

74. Adrenergic receptors in human veins. Full Text available with Trip Pro

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

1970 Canadian Medical Association Journal

75. Responses of coronary vessels to adrenergic stimuli Full Text available with Trip Pro

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

1971 Journal of Clinical Investigation

76. Ectopic beta-adrenergic receptor binding sites. possible molecular basis of aberrant catecholamine responsiveness of an adrenocortical tumor adenylate cyclase. Full Text available with Trip Pro

] 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

1977 Journal of Clinical Investigation

77. The effects of labetalol (AH 5158) on adrenergic transmission in the cat spleen. Full Text available with Trip Pro

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.

1977 British journal of pharmacology

78. Characterization of the Human Platelet α-Adrenergic Receptor: CORRELATION OF [3H] DIHYDROERGOCRYPTINE BINDING WITH AGGREGATION AND ADENYLATE CYCLASE INHIBITION Full Text available with Trip Pro

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

1978 Journal of Clinical Investigation

79. Selective labeling of α-adrenergic receptors in caudate nucleus by [3H]dihydroergocryptine in the presence of spiperone-blocked dopamine receptors Full Text available with Trip Pro

) 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

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

80. Pulmonary Alveolar Type II Cells Isolated from Rats: RELEASE OF PHOSPHATIDYLCHOLINE IN RESPONSE TO β-ADRENERGIC STIMULATION Full Text available with Trip Pro

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

1979 Journal of Clinical Investigation

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