Relevant bibliographies by topics / [beta]2-adrenoceptor agonist drugs

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters

Academic literature on the topic '[beta]2-adrenoceptor agonist drugs'

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Published: 19 February 2023

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Journal articles on the topic "[beta]2-adrenoceptor agonist drugs"

1

Folkow, L. P. "Adrenergic vasomotor responses in nasal mucosa of hooded seals." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 263, no. 6 (December 1, 1992): R1291—R1297. http://dx.doi.org/10.1152/ajpregu.1992.263.6.r1291.

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In seals respiratory heat and water losses are restricted through nasal heat exchange. The heat exchange efficiency is apparently controlled through adjustments in the nasal mucosal blood flow rate and/or pattern. In this study the adrenergic mechanisms involved in regulation of mucosal blood flow were investigated. The nasal mucosal vasculature of 14 newly killed hooded seal (Cystophora cristata) pups was perfused by a constant-flow peristaltic pump with 37 degrees C oxygenated modified Krebs solution via the sphenopalatine arteries. The effects of single-dose injections of various drugs on resistance to flow were monitored with a pressure transducer. Epinephrine, norepinephrine, alpha 1-adrenoceptor agonist phenylephrine, alpha 2-agonist clonidine, beta 1-agonist dobutamine, and beta 2-agonist terbutaline caused transient pressure increases that were blocked by alpha-adrenoceptor antagonists. Papaverine and vasoactive intestinal polypeptide induced vasodilatation, showing that some basal vascular tone was present. Nevertheless, the beta 1- and beta 2-agonist isoproterenol had no effect on resistance, and none of the beta-agonists attenuated the pressor responses to alpha-agonists. In conclusion, adrenergic control of nasal mucosal blood flow in seals is essentially exerted through alpha-adrenoceptor-mediated arteriolar constriction, whereas beta-adrenoceptor-mediated dilatation seems to be of little importance. It is suggested that such sympathoadrenergic vascular mechanisms contribute to control nasal heat exchange efficiency in seals.
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2

Tavernier, G., J. Galitzky, P. Valet, A. Remaury, A. Bouloumie, M. Lafontan, and D. Langin. "Molecular mechanisms underlying regional variations of catecholamine-induced lipolysis in rat adipocytes." American Journal of Physiology-Endocrinology and Metabolism 268, no. 6 (June 1, 1995): E1135—E1142. http://dx.doi.org/10.1152/ajpendo.1995.268.6.e1135.

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The mechanisms underlying catecholamine control of lipolysis were studied in rat white adipocytes from epididymal, retroperitoneal, and subcutaneous fat depots. Sensitivity of subcutaneous adipocytes to selective beta 3-adrenoceptor agonists was lower than that of internal adipocytes. beta 3-Adrenoceptor mRNA levels were lower in subcutaneous adipocytes. A decreased beta 1/beta 2-adrenoceptor-mediated lipolysis was also observed in these adipocytes, and the number of beta 1/beta 2-adrenoceptors was lower than in the internal adipocytes. The number of alpha 2-adrenoceptors was higher in subcutaneous adipocytes without a marked difference in alpha 2-adrenoceptor-mediated antilipolysis between the depots. Subcutaneous adipocytes were also characterized by a lower maximal lipolytic response to drugs acting at different levels of the lipolytic cascade, suggesting differences at the postreceptor level. Lower hormone-sensitive lipase activity and mRNA levels in subcutaneous adipocytes were in agreement with the lipolysis data. These results suggest that the pattern of expression of the genes of the lipolytic pathway varies with the anatomic location of the fat depot.
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Lofdahl, CG, and KF Chung. "Long-acting beta 2-adrenoceptor agonists: a new perspective in the treatment of asthma." European Respiratory Journal 4, no. 2 (February 1, 1991): 218–26. http://dx.doi.org/10.1183/09031936.93.04020218.

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New long-acting beta 2-adrenoceptor agonists, formoterol and salmeterol, may soon appear in several European countries for treatment of asthma. This review examines currently available information and compares the basic pharmacology and describes the clinical effects of these new drugs. The long duration of bronchodilation seen in clinical studies seems to be similar, whereas in isolated tissues there might be a difference in the binding characteristics to the beta 2-adrenoceptor. Long-acting beta 2-agonists could have an inhibitory effect on inflammatory events related to asthma, but the clinical relevance of these effects is not clear at present. Long-term studies up to one year with both new drugs have not shown any unexpected side-effects, and no tachyphylaxis to beta-adrenoceptor stimulation has been reported. Patients appear to strongly prefer the new drugs compared to the short-acting beta 2-agonists. The potential place for these drugs in the treatment of asthma is discussed and some pitfalls pointed out. It is likely that the long-acting beta 2-agonists will be beneficial to many asthmatic patients.
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Ulrik, CS, and A. Kok-Jensen. "Different bronchodilating effect of salmeterol and formoterol in an adult asthmatic." European Respiratory Journal 7, no. 5 (May 1, 1994): 1003–5. http://dx.doi.org/10.1183/09031936.94.07051003.

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New long-acting beta 2-adrenoceptor agonists, salmeterol and formoterol, have recently been marketed for treatment of asthma, but studies comparing the clinical efficacy of the two drugs have not been published. We report on an asthmatic patient who had a striking difference in bronchodilating effect of the two drugs, formoterol being more effective than salmeterol both in immediate response and during long-term treatment. Although, both formoterol and salmeterol are highly selective for the beta 2-adrenoceptors (comparable to salbutamol and terbutaline), differences in their chemical structure suggest differences in their mechanisms of action or receptor specificity. The clinical implication of our observation appears to be that a less favourable response in an individual patient to one of the long-acting beta 2-agonists should not preclude a trial with another. Future studies comparing the clinical efficacy of formoterol and salmeterol should probably also address the question of responders and nonresponders to these drugs; and furthermore, seek to explore a possible relationship to inherited variance in beta 2-receptors.
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5

al-Damluji, S., and D. Francis. "Activation of central alpha 1-adrenoceptors in humans stimulates secretion of prolactin and TSH, as well as ACTH." American Journal of Physiology-Endocrinology and Metabolism 264, no. 2 (February 1, 1993): E208—E214. http://dx.doi.org/10.1152/ajpendo.1993.264.2.e208.

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In normal male volunteers, intravenous infusions of the alpha 1-adrenergic agonist methoxamine stimulated the secretion of prolactin, thyroid-stimulating hormone (TSH), and adrenocorticotropic hormone (ACTH), and the effects were abolished by pretreatment with the alpha 1-antagonist prazosin. To investigate the site of action of methoxamine, its effects were compared with those of equipotent doses of norepinephrine, an alpha 1-agonist that reaches the pituitary gland and the median eminence after an intravenous infusion but, unlike methoxamine, does not cross the blood-brain barrier. Norepinephrine did not stimulate secretion of prolactin, TSH, or ACTH, suggesting that the stimulant alpha 1-adrenoceptors are located in the central nervous system and not directly on the pituitary gland or in the periphery. The alpha 2- and beta-adrenoceptor agonist properties of norepinephrine could not account for the differences from methoxamine, as pretreatment with prazosin did not modify hormone concentrations after norepinephrine. Methoxamine had no behavioral stimulant effects, as judged by visual analog scales that were sensitive to physiological changes in behavioral arousal. In four patients with hypothalamic dysfunction but responsive pituitary corticotrophs, methoxamine had no stimulant effect on the secretion of ACTH, confirming that the alpha 1-adrenoceptors that stimulate ACTH secretion are not located directly on the pituitary. None of the drugs had an effect on the secretion of growth hormone or the gonadotrophins.
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6

Moore, N. G., G. G. Pegg, and M. N. Sillence. "Anabolic effects of the beta 2-adrenoceptor agonist salmeterol are dependent on route of administration." American Journal of Physiology-Endocrinology and Metabolism 267, no. 3 (September 1, 1994): E475—E484. http://dx.doi.org/10.1152/ajpendo.1994.267.3.e475.

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It is reported that a long duration of action is required for beta 2-adrenoceptor agonists to evoke an anabolic response. In the present study, we compare the potency of clenbuterol with that of the new long-acting compound salmeterol, when given at equimolar doses to female Wistar rats by different routes of administration. Given orally for 10 days, salmeterol had no effect on growth at a dose of 120 micrograms/day, whereas at 2.4 mg/day the drug caused significant increases in body and carcass weight and in the mass of the mixed-fiber gastrocnemius/plantaris and tibialis anterior muscles, but there were no increases in the slow-twitch soleus muscles. A similar growth response was seen when clenbuterol was given orally at a dose of only 97 micrograms/day, with an additional response seen in soleus muscle at 1.9 mg/day. Thus clenbuterol was more potent than salmeterol when given by this route of administration. When the drugs were infused by osmotic minipump, both salmeterol (130 micrograms/day) and clenbuterol (100 micrograms/day) caused increases in body weight gain and in the weights of the mixed-fiber muscles, with the most dramatic effect of infusion being to greatly increase the anabolic effect of salmeterol in soleus muscle. A single intraperitoneal injection of salmeterol (53 micrograms) or clenbuterol (40 micrograms) caused a similar rapid increase in the concentration of adenosine 3',5'-cyclic monophosphate in gastrocnemius muscle. These results indicate that the potency of salmeterol in vivo is dependent on its route of administration and that slow-twitch muscles are less sensitive than mixed-fiber muscles to the anabolic effects of beta 2-adrenoceptor agonists.
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García-Lunar, Inés, Daniel Pereda, Borja Ibanez, and Ana García-Álvarez. "Neurohormonal Modulation as a Therapeutic Target in Pulmonary Hypertension." Cells 9, no. 11 (November 22, 2020): 2521. http://dx.doi.org/10.3390/cells9112521.

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The autonomic nervous system (ANS) and renin-angiotensin-aldosterone system (RAAS) are involved in many cardiovascular disorders, including pulmonary hypertension (PH). The current review focuses on the role of the ANS and RAAS activation in PH and updated evidence of potential therapies targeting both systems in this condition, particularly in Groups 1 and 2. State of the art knowledge in preclinical and clinical use of pharmacologic drugs (beta-blockers, beta-three adrenoceptor agonists, or renin-angiotensin-aldosterone signaling drugs) and invasive procedures, such as pulmonary artery denervation, is provided.
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Janson, C., J. Boe, G. Boman, B. Mossberg, and N. Svedmyr. "Bronchodilator intake and plasma levels on admission for severe acute asthma." European Respiratory Journal 5, no. 1 (January 1, 1992): 80–85. http://dx.doi.org/10.1183/09031936.93.05010080.

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We have measured the plasma levels of salbutamol, terbutaline and theophylline in 140 patients (70 men, mean age 57 yrs) arriving for emergency treatment with severe acute asthma. The aim of the study was to investigate how the measured plasma levels correlated with the reported bronchodilator intake and whether the pretreatment beta 2-agonist levels influenced the effect of emergency salbutamol treatment. We found a highly significant correlation between the reported 24 h dose and the measured plasma concentrations for all three drugs. A plasma concentration less than 40 mumol.l-1 was found in 63 of the 107 patients who had taken theophylline, while no patient had a plasma concentration greater than 110 mumol.l-1. A plasma concentration above the suggested therapeutic range was found in 23 of the 95 patients who had taken terbutaline (greater than 30 nmol.l-1) and in 12 of the 98 patients who had taken salbutamol (greater than 60 nmol.l-1). A significant negative correlation was found between the initial plasma beta 2-agonist levels and the bronchodilation after i.v. salbutamol treatment (5 micrograms.kg-1), while there was no clear indication that high plasma beta 2-agonist levels reduced the bronchodilator effect of a high dose of inhaled salbutamol (0.15 mg.kg-1 x 2). We conclude that some patients arriving with acute asthma have high blood concentrations of beta 2-agonists, which possibly limit the response to i.v. beta 2-agonist treatment, while the effect of high-dose inhaled beta 2-agonists appears to be related to a lesser degree to the drug concentration on arrival. In this study overtreatment with theophylline appears to be uncommon.
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Lammers, JW, ME Muller, HT Folgering, and CL van Herwaarden. "Effects of terbutaline and atenolol on large and small airways in asthmatic patients." European Respiratory Journal 1, no. 5 (May 1, 1988): 453–57. http://dx.doi.org/10.1183/09031936.93.01050453.

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In order to localize the main site of action of the beta 2-adrenoceptor selective agonist terbutaline and the beta 1-adrenoceptor selective antagonist atenolol in the airways of asthmatic patients, we compared the effects of these drugs on maximal expiratory flow-volume (MEFV) curves when breathing air and when breathing a helium-oxygen (HeO2) mixture. To investigate whether a shift in localization of the bronchodilator effect occurs when terbutaline is inhaled repeatedly, dose-response curves with terbutaline were performed for parameters derived from MEFV curves when breathing air and for density dependence of expiratory airflow. By measurement of MEFV curves when the patients were breathing air alone, it was not possible to determine whether there is a difference in the bronchoconstrictor effect of atenolol between large and small airways. Inhalation of terbutaline to a cumulative dose of 2.0 mg induced a stepwise improvement in expiratory airflow parameters for large and small airways function when breathing air. Doubling the dose of inhaled terbutaline to 4 mg did not result in any further improvement of lung function. Neither atenolol nor terbutaline induced significant mean changes in density dependence of expiratory airflow. This was partly due to large inter- and intra-individual variations of this parameter. Another possibility is that atenolol and terbutaline effect large and small airways function equally.
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10

Naline, E., Y. Zhang, Y. Qian, N. Mairon, GP Anderson, B. Grandordy, and C. Advenier. "Relaxant effects and durations of action of formoterol and salmeterol on the isolated human bronchus." European Respiratory Journal 7, no. 5 (May 1, 1994): 914–20. http://dx.doi.org/10.1183/09031936.94.07050914.

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The objective of this study was to evaluate the potency and efficacy (intrinsic activity) of formoterol and salmeterol and their duration of action in comparison with other beta-adrenoceptor agonists in isolated human bronchi. Human bronchi were obtained at thoracotomy from patients with lung cancer. Potency (-log of the concentration of drug inducing 50% of maximal relaxation (-log EC50)) and efficacy (maximal effect (Emax), % of response to theophylline 3 x 10(-3) mol.l-1) were determined by analysis of cumulative isometric concentration-response curves to beta 2-adrenoceptor agonists in bronchial rings at resting tone or contracted maximally with acetylcholine 10(-3) mol.l-1 to induce functional antagonism. The onset and duration of action of beta-adrenoceptor agonists were measured by assessing the relaxant activity of drugs on the basal tone of isolated bronchi. In terms of potency, the rank order of the substances studied was formoterol > fenoterol > or = salmeterol > or = isoprenaline > or = salbutamol > or = adrenaline > or = terbutaline. Formoterol was 150-200 times more potent than isoprenaline. On preparations contracted with acetylcholine 10(-3) mol.l-1 the intrinsic activity (IA) of salbutamol, terbutaline and salmeterol compared with that of isoprenaline ranged 0.62-0.66. Intrinsic activity was higher with formoterol (0.84) and fenoterol (0.75). The onset of action of formoterol (2.14 +/- 0.55 min, n = 11) was not significantly different from that of salbutamol (1.90 +/- 0.24 min, n = 8) but shorter than that of salmeterol (6.40 +/- 1.40 min, n = 10).(ABSTRACT TRUNCATED AT 250 WORDS)
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Dissertations / Theses on the topic "[beta]2-adrenoceptor agonist drugs"

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Lortie, Michel B. "The rainbow trout muscle beta(2)-adrenoceptor system: Impact of beta(2)-agonist feeding." Thesis, University of Ottawa (Canada), 2002. http://hdl.handle.net/10393/6268.

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Previous studies showed that beta2-adrenergic agonists (beta 2-AAs) enhanced muscle growth and reduced lipid deposition in animals of agricultural and economical importance, including teleost fish. The goal of the present study was to provide a mechanistic explanation underlying the reported beta2-AA-induced muscle growth in the rainbow trout (Oncorhynchus mykiss). Using radioligand binding assays and adenylyl cyclase/cAMP assays, this study characterized and demonstrated the presence of functional beta2-adrenoceptors (beta2-ARs) on red and white muscle membranes. Trout fed 40 ppm of two beta2-AAs (clenbuterol and ractopamine) for 30 days showed no significant changes in measured body and physiological parameters, beta2-AR numbers or beta2-AR mRNA levels in red or white muscle. However, treatments significantly increased fractional protein synthesis rates in red and white muscle. These studies demonstrate that beta2-AAs impact muscle protein synthesis by mechanisms initiated at the muscle membrane beta 2-AR and include the beta2-AR-signalling pathway in a teleost fish.
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2

(9630230), RA Hill. "Development of a [beta]-adrenoceptor vaccine." Thesis, 1994. https://figshare.com/articles/thesis/Development_of_a_beta_-adrenoceptor_vaccine/13422584.

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Aim of the project is to demonstrate that antibodies could be used to activate the [Beta]-adrenoceptor ([Beta]-AR). Identifying a candidate vaccine suitable for administration to cattle which would evoke the production of such antibodies in also investigated.. The efficiency of cattle growth can be enhanced by the use of ß2-adrenoceptor agonist drugs. How-ever, synthetic drugs are not acceptable for use in animal production, and an alternative, immuno-logical manipulation, has been proposed. Thus, one aim of this project was to demonstrate that antibodies could be used to activate the ß2-adrenoceptor (ß2-AR). A second aim was to identify a candidate vaccine suitable for administration to cattle, which would evoke the production of such antibodies. Two vaccine approaches were investigated. Transgenic Escherichia coli which express the human ß2-AR provided one potential source of antigen. However, attempts to affinity purify 2-AR from digitonin solubilised E. coli were unsuccessful. Synthetic peptides were utilised as the second source of antigen. Two of these peptides corresponded to all (24 amino acids) or the N-terminal part (13 amino acids) of the second outer loop of the human ß2-AR. These were designated H24T and H 13C respectively. The third peptide was the bovine homologue of H24T, and was designated bov-H24T accordingly. H24T was highly immunogenic, causing maximum titres assayed by ELISA of 160000 in mice, and 10000 in rabbits and cattle. H13C, was used to immunise mice and rabbits, but evoked antibodies in rabbits only, the maximal titre being about 10000. These results allowed a mouse B epitope on H24T to be partially mapped to positions 185-187 (-Y-A-N-) on the human ß2-AR. Cattle were also immunised with bov-H24T. This peptide was also highly immunogenic, titres rising to a maximum of 12000. Rabbit and bovine antibodies were affinity purified and screened in a number of assays in vitro to determine their interaction with ß₂-AR. Anti-H24T antibodies from three rabbits recognised human ß2-AR, showing some cross-reaction with human ß1- and ß3-AR as determined in immunoblots. Antibodies from one rabbit were investigated further. They were found to increase the affinity of the radioligand [¹²⁵l]- iodocyanopindolol for bovine skeletal muscle ß2-AR. Both rabbit and bovine antibodies induced c-AMP production in rat skeletal muscle at concentrations as low as 1 pM, and increased the potency of isoprenaline in bovine tracheal smooth muscle. This is the first time that anti-ß2-AR antibodies have been shown to evoke a functional response. Thus, it has been shown that antibodies which activate ß2-AR can be raised in cattle in response to a synthetic peptide antigen. Further work will be needed to establish whether this vaccine will mimic the effects of a ß2-agonist drug by increasing the carcase muscle to fat ratio in treated cattle, and whether it is a technology likely to be adopted by the Australian beef industry.
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"GLP-1 receptor agonist exendin-4 improves glycemic control through beta cell and non-beta cell mechanism." Thesis, 2011. http://library.cuhk.edu.hk/record=b6075398.

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Fan, Rongrong.
Thesis (Ph.D.)--Chinese University of Hong Kong, 2011.
Includes bibliographical references (leaves 130-150).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstract also in Chinese.
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Books on the topic "[beta]2-adrenoceptor agonist drugs"

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Friedrich, Kummer, and Vienna Asthma Forum (6th : 1996), eds. Treatment of asthma: The long-acting beta-2-agonists. Wien: Springer-Verlag, 1998.

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1946-, Frishman William H., ed. Beta₃-adrenergic agonism: A new concept in human pharmacotherapy. Armonk, N.Y: Futura, 1995.

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Berger, W., R. Flückiger, H. G. Köppe, K. T. Holmes, C. E. Mountford, E. L. Nickoloff, T. G. Payne, M. H. Schreier, I. C. P. Smith, and R. M. Wenger. Metabolic Control in Diabetes Mellitus Beta Adrenoceptor Blocking Drugs NMR Analysis of Cancer Cells Immunoassay in the Clinical Laboratory Cyclosporine. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-70998-2.

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Johnson, Malcolm, and Roger Small. Beta-Adrenoceptor Agonists and the Airways. Royal Society of Medicine Press Ltd, 1995.

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Dr, Johnson Malcolm, Small Roger, British Pharmacological Society Meeting, and Glaxo Group Research Limited, eds. [Beta]-adrenoceptor agonists and the airways: Held as satellite meeting to the British Pharmacological Society Meeting, School of Biological Sciences, University of Manchester, 12-15 April 1994. London: Royal Society of Medicine Press, 1995.

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(Editor), Friedrich Kummer, and Vienna Asthma Forum 1996 (Editor), eds. Treatment of Asthma: The Long-Acting Beta-2-Agonists. Springer, 1998.

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Kummer, Friedrich. Treatment of Asthma: The Long-Acting Beta-2-agonists. Springer London, Limited, 2012.

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(Editor), Romain Pauwels, and Paul O'Byrne (Editor), eds. Beta 2-agonists in Asthma Treatment (Lung Biology in Health and Disease). Informa Healthcare, 1997.

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Frishman, William H., and Daniel E. Goldberg. Beta3 Adrenergic Agonism: A New Concept in Human Pharmacotherapy. Futura Publishing Company, 1995.

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1946-, Barnes Peter J., Matthys Heinrich, and European Society of Pneumology. Congress, eds. Formoterol--a new-generation [beta] 2-agonist: An international symposium held during the 8th Congress of the European Society of Pneumology, Freiburg, Federal Republic of Germany, September 1989. Toronto: Hogrefe & Huber, 1991.

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Book chapters on the topic "[beta]2-adrenoceptor agonist drugs"

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Newbold, Paul, Dale M. Jackson, Alan Young, Iain G. Dougall, Frank Ince, Karen M. S. Rocchiccioli, and Phil R. Holt. "Dual D2 Dopamine Receptor and β2-Adrenoceptor Agonists for the Modulation of Sensory Nerves in COPD." In New Drugs for Asthma, Allergy and COPD, 68–71. Basel: KARGER, 2001. http://dx.doi.org/10.1159/000062134.

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Schöni, M. H. "The Beta — 2 — Agonist Perplexity: Pro and Contra Sympathomimetic Drugs in Childhood Asthma." In Update on Childhood Asthma, 191–200. Basel: Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-7385-7_15.

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Chester, Neil, and David R. Mottram. "Beta-2 agonists." In Drugs in Sport, 173–87. Seventh edition. | Milton Park, Abingdon ; New York, NY : Routledge, 2018.: Routledge, 2018. http://dx.doi.org/10.4324/9781315222790-11.

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Chester, Neil, and David Mottram. "Beta-2 agonists." In Drugs in Sport, 186–201. 8th ed. London: Routledge, 2021. http://dx.doi.org/10.4324/9781003096160-12.

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Johnson, Malcolm, and Gerry W. E. Hagan. "Long-Acting β2-Agonists." In New Drugs for Asthma, Allergy and COPD, 60–63. Basel: KARGER, 2001. http://dx.doi.org/10.1159/000062130.

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Anderson, Gary P. "Long Acting Inhaled Beta-Adrenoceptor Agonists the Comparative Pharmacology of Formoterol and Salmeterol." In New Drugs in Allergy and Asthma, 253–69. Basel: Birkhäuser Basel, 1993. http://dx.doi.org/10.1007/978-3-0348-7324-6_22.

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Beier, Jutta, Alexandre Trifilieff, and Mark Higgins. "Indacaterol: A new once-daily long-acting β2-adrenoceptor agonist (LABA)." In New Drugs and Targets for Asthma and COPD, 27–31. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320795.

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O’Donnell, Stella R. "The Development of Beta Receptor Agonist Drugs." In The Role of Beta Receptor Agonist Therapy in Asthma Mortality, 3–26. CRC Press, 2020. http://dx.doi.org/10.1201/9780429281082-2.

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"Beta2-adrenoceptor agonists." In Meyler's Side Effects of Drugs: The International Encyclopedia of Adverse Drug Reactions and Interactions, 448–52. Elsevier, 2006. http://dx.doi.org/10.1016/b0-44-451005-2/01322-x.

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"Beta2-adrenoceptor agonists." In Meyler's Side Effects of Drugs, 889–96. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-444-53717-1.00379-6.

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