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Journal articles on the topic 'Beta agonist'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Brechet, S., P. Plaisancie, V. Dumoulin, JA Chayvialle, JC Cuber, and J. Claustre. "Involvement of beta1- and beta2- but not beta3-adrenoceptor activation in adrenergic PYY secretion from the isolated colon." Journal of Endocrinology 168, no. 1 (2001): 177–83. http://dx.doi.org/10.1677/joe.0.1680177.

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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 transi

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2

Sears, Malcolm R. "Short-Acting Beta-Agonist Research: A Perspective." Canadian Respiratory Journal 8, no. 5 (2001): 349–55. http://dx.doi.org/10.1155/2001/987151.

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Asthma mortality increased sharply in New Zealand in 1977, prompting a national investigation into circumstances of asthma deaths. Subsequent observations of improved asthma control in subjects withdrawn from regular beta2-agonist treatment raised the question of whether asthma severity and, therefore, mortality could relate to frequent beta-agonist use. A randomized controlled trial of regular inhaled fenoterol versus as-needed bronchodilator use showed worsened asthma control during regular treatment despite concomitant use of inhaled corticosteroids. Assessment of these findings led to dela

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3

Mio, T., Y. Adachi, S. Carnevali, D. J. Romberger, J. R. Spurzem, and S. I. Rennard. "Beta-adrenergic agonists attenuate fibroblast-mediated contraction of released collagen gels." American Journal of Physiology-Lung Cellular and Molecular Physiology 270, no. 5 (1996): L829—L835. http://dx.doi.org/10.1152/ajplung.1996.270.5.l829.

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The effects of beta-adrenergic agonists on fibroblast-mediated collagen gel contraction were investigated. beta-Agonists isoproterenol and epinephrine significantly attenuated fibroblast-mediated gel contraction in a concentration-dependent manner, whereas alpha-agonist norepinephrine had no effect. The biologically active form of isoproterenol, (-)-isoproterenol, was 10-fold more effective than the optical isoform, (+)-isoproterenol. beta-Antagonists sotalol and propranolol reversed the attenuation caused by 10(-7) M isoproterenol or epinephrine at the concentration of 10(-7) M or 10(-6) M, b

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4

Kelly, H. William, and Shirley Murphy. "Beta-Adrenergic Agonists for Acute, Severe Asthma." Annals of Pharmacotherapy 26, no. 1 (1992): 81–91. http://dx.doi.org/10.1177/106002809202600115.

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OBJECTIVE: To critically review the use of beta-adrenergic agonists in acute, severe asthma with particular focus on aerosol administration. DATA SOURCES: English language articles published since 1971 on the use of beta-agonists for acute asthma. Studies were identified from bibliographies of book chapters, review articles, and other research articles. STUDY SELECTION: All studies (21 total) comparing systemic with inhaled beta-agonists were reviewed, regardless of their design or outcome. Selected studies highlighting specific aspects of beta-agonist use in acute asthma such as beta-agonists

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5

Wang, H. Y., M. Berrios та C. C. Malbon. "Localization of β-adrenergic receptors in A431 cells in situ. Effect of chronic exposure to agonist". Biochemical Journal 263, № 2 (1989): 533–38. http://dx.doi.org/10.1042/bj2630533.

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The status of beta-adrenergic receptors was investigated in A431 cells exposed to chronic stimulation by the beta-adrenergic agonist, (-)-isoproterenol. Specific binding of beta-adrenergic antagonist (-)-[125I]iodocyanopindolol declined to 60-80% below control values within 12 h of agonist treatment. This decline in ligand binding was also observed in high-speed membrane fractions prepared from agonist-treated cells. Immunoblots probed with anti-receptor antibodies revealed both that beta-adrenergic receptors from untreated and treated cells migrated as 65,000-Mr peptides and that the cellular

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6

Folkow, L. P. "Adrenergic vasomotor responses in nasal mucosa of hooded seals." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 263, no. 6 (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 r

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7

Taylor, D. Robin, Malcolm R. Sears, and Donald W. Cockcroft. "THE BETA-AGONIST CONTROVERSY." Medical Clinics of North America 80, no. 4 (1996): 719–48. http://dx.doi.org/10.1016/s0025-7125(05)70465-x.

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8

&NA;. "Beta agonist controversy continues." Inpharma Weekly &NA;, no. 827 (1992): 6. http://dx.doi.org/10.2165/00128413-199208270-00005.

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9

&NA;. "The beta agonist battle." Inpharma Weekly &NA;, no. 826 (1992): 18. http://dx.doi.org/10.2165/00128413-199208260-00035.

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10

McIntyre, Chelsey M., and Patricia-Ann Betts. "Long-Acting Beta Agonist." Journal of Asthma & Allergy Educators 3, no. 3 (2012): 127–28. http://dx.doi.org/10.1177/2150129712443555.

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11

Ziment, Irwin. "Beta-adrenergic Agonist Toxicity." Chest 103, no. 5 (1993): 1591–97. http://dx.doi.org/10.1378/chest.103.5.1591.

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12

McKinney, J. S., M. S. Desole, and R. P. Rubin. "Convergence of cAMP and phosphoinositide pathways during rat parotid secretion." American Journal of Physiology-Cell Physiology 257, no. 4 (1989): C651—C657. http://dx.doi.org/10.1152/ajpcell.1989.257.4.c651.

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Rat parotid acinar cells were employed to investigate the mechanism by which receptor agonists that activate the phosphoinositide pathway enhance the stimulatory effects of adenosine 3',5'-cyclic monophosphate (cAMP) on amylase secretion. Norepinephrine (NE), which activates both alpha- and beta-adrenoceptors, evoked a secretory response that was greater than the sum of the responses obtained when NE was employed as a beta-agonist (in the presence of prazosin) and as an alpha-agonist (in the presence of propranolol). The enhancement of amylase secretion induced by NE was accompanied by an augm

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13

Ayala, A., and F. Kierszenbaum. "Regulation of Trypanosoma cruzi infectivity by alpha- and beta-adrenergic agonists: desensitization produced by prolonged treatments or increasing agonist concentrations." Parasitology 100, no. 3 (1990): 429–34. http://dx.doi.org/10.1017/s0031182000078720.

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SUMMARYWe previously reported that blood forms of Trypanosoma cruzi express alpha- and beta-adrenergic receptors and that binding of specific agonists to these receptors modifies the infective capacity of the parasite in vitro. The present study has revealed that the inhibitory effect of the beta-adrenergic agonist L-isoproterenol and the stimulatory effect of the alpha-adrenergic agonist L-phenylephrine are not produced when the parasite is subjected to prolonged exposure to otherwise effective doses of these agonists or when supraoptimal doses of these agonists are used. We refer to these ph

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14

Petrovic, S. L., J. C. Bedran De Castro, and S. M. McCann. "Beta-adrenergic agonists increase amplitude of LH release in orchidectomized rats." American Journal of Physiology-Endocrinology and Metabolism 251, no. 3 (1986): E316—E321. http://dx.doi.org/10.1152/ajpendo.1986.251.3.e316.

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The role of intravenously (iv) injected adrenergic agonists in the pulsatile secretion of luteinizing hormone (LH) was examined in unanesthesized, freely behaving, castrated male rats. The alpha 2-adrenergic receptor agonist, clonidine (25 micrograms/kg), and the alpha 1-adrenergic agonist, (-)-phenylephrine (12.5 micrograms/kg), did not significantly alter pulsatile release of LH. The physiological beta 2-adrenergic receptor agonist, (-)-epinephrine (2.5 micrograms/kg), significantly increased the mean plasma concentrations of plasma LH and the amplitude of the LH pulses over a period of 70 m

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15

Meyer, Joette M., Christine L. Wenzel, and Wayne A. Kradjan. "Salmeterol: A Novel, Long-Acting Beta2-Agonist." Annals of Pharmacotherapy 27, no. 12 (1993): 1478–87. http://dx.doi.org/10.1177/106002809302701214.

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OBJECTIVE: The clinical pharmacology, pharmacokinetics, clinical efficacy, and adverse effects of the long-acting beta2-agonist salmeterol are reviewed. DATA SOURCES: A MEDLINE search was performed to identify English-language publications pertaining to salmeterol. STUDY SELECTION: Open and controlled trials were reviewed in assessing clinical efficacy. Only the results of controlled, randomized trials were considered in the effectiveness evaluation. DATA EXTRACTION: The primary measures of effectiveness in the clinical trials were bronchodilator activity and reduction of hyperresponsiveness t

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16

Carpene, C., I. Castan, P. Collon, J. Galitzky, J. Moratinos, and M. Lafontan. "Adrenergic lipolysis in guinea pig is not a beta 3-adrenergic response: comparison with human adipocytes." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 266, no. 3 (1994): R905—R913. http://dx.doi.org/10.1152/ajpregu.1994.266.3.r905.

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beta 3-Adrenoceptor agonists are potent lipolytic activators in rats, but they are only weak stimulators in human adipocytes, indicating interspecies differences in the adrenergic regulation of lipid mobilization. Like human but not rat adipocytes, guinea pig fat cells were poorly responsive to the beta 3-agonists BRL-37344, CGP-12177, SR-58611, and ICI-215001, acid metabolite of ICI-D7114. In guinea pigs, the beta 1-agonist dobutamine was more lipolytic than the beta 2-agonist procaterol. Anatomic location of fat deposits was without major influence on the beta-adrenergic responsiveness. Weak

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17

Riis-Vestergaard, Mette Ji, Bjørn Richelsen, Jens Meldgaard Bruun, Wei Li, Jacob B. Hansen, and Steen Bønløkke Pedersen. "Beta-1 and Not Beta-3 Adrenergic Receptors May Be the Primary Regulator of Human Brown Adipocyte Metabolism." Journal of Clinical Endocrinology & Metabolism 105, no. 4 (2019): e994-e1005. http://dx.doi.org/10.1210/clinem/dgz298.

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Abstract Purpose Brown adipose tissue (BAT) activation in humans has gained interest as a potential target for treatment of obesity and insulin resistance. In rodents, BAT is primarily induced through beta-3 adrenergic receptor (ADRB3) stimulation, whereas the primary beta adrenergic receptors (ADRBs) involved in human BAT activation are debated. We evaluated the importance of different ADRB subtypes for uncoupling protein 1 (UCP1) induction in human brown adipocytes. Methods A human BAT cell model (TERT-hBA) was investigated for subtype-specific ADRB agonists and receptor knockdown on UCP1 mR

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18

Zeman, R. J., Y. Zhang, and J. D. Etlinger. "Clenbuterol, a beta 2-agonist, retards wasting and loss of contractility in irradiated dystrophic mdx muscle." American Journal of Physiology-Cell Physiology 267, no. 3 (1994): C865—C868. http://dx.doi.org/10.1152/ajpcell.1994.267.3.c865.

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Treatment with the adrenergic beta 2-receptor agonist clenbuterol prevented, in dystrophic muscle from mdx mice, a pronounced loss of contractile strength that is observed after blockade of muscle regeneration with gamma irradiation. In addition, muscle mass and myosin content were greater (62-109%) in irradiated hindlimbs from clenbuterol-treated mdx mice, whereas the effects of the beta 2-agonist were relatively smaller (12-21%) in the nonirradiated hindlimbs. Together, these results suggest that beta 2-agonists can antagonize degenerative processes occurring in muscle fibers lacking dystrop

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19

Carpene, C., L. Ambid, and M. Lafontan. "Predominance of beta 3-adrenergic component in catecholamine activation of lipolysis in garden dormouse adipocytes." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 266, no. 3 (1994): R896—R904. http://dx.doi.org/10.1152/ajpregu.1994.266.3.r896.

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The beta 3-adrenoceptor (AR) agonists are potent activators of lipolysis in white adipose tissue. beta-AR agonists were tested here on the lipolytic activity of a hibernator, the garden dormouse (Eliomys quercinus L.). All the agonists exhibited full intrinsic activity; the most potent was the beta 3-AR agonist BRL-37344 [half-maximal effective concentration (EC50) = 0.8 nM]. The beta-antagonist idocyanopindolol (ICYP) also stimulated lipolysis of white adipocytes with the same potency and intrinsic activity as BRL-37344. The blockade of lipolytic effects of epinephrine or norepinephrine was s

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20

Pearlman, David S. "High Beta-Agonist Users in Five HMOs: Implications Beyond High Beta-Agonist Use." Annals of Allergy, Asthma & Immunology 76, no. 2 (1996): 125–27. http://dx.doi.org/10.1016/s1081-1206(10)63410-2.

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21

Turki, J., S. A. Green, K. B. Newman, M. A. Meyers, and S. B. Liggett. "Human lung cell beta 2-adrenergic receptors desensitize in response to in vivo administered beta-agonist." American Journal of Physiology-Lung Cellular and Molecular Physiology 269, no. 5 (1995): L709—L714. http://dx.doi.org/10.1152/ajplung.1995.269.5.l709.

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Few studies have addressed whether target tissue adrenergic receptors in humans undergo desensitization in response to agonist administration. To determine whether lung cell beta 2-adrenergic receptors (beta 2-AR) undergo such desensitization, we harvested bronchial epithelial cells and alveolar macrophages via bronchoscopy from eight normal subjects before and after inhalation of six doses of the beta-agonist metaproterenol given over 24 h. After metaproterenol inhalation, beta 2-AR expression as determined by 125I-labeled cyanopindolol binding decreased approximately 70% on bronchial epithel

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22

Penn, R. B., J. R. Shaver, J. G. Zangrilli, et al. "Effects of inflammation and acute beta-agonist inhalation on beta 2-AR signaling in human airways." American Journal of Physiology-Lung Cellular and Molecular Physiology 271, no. 4 (1996): L601—L608. http://dx.doi.org/10.1152/ajplung.1996.271.4.l601.

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Although alterations in beta 2-adrenergic receptor (AR) responsiveness may in part explain reports linking deterioration of asthma control with beta-agonist treatment of asthmatics, few data exist on beta 2-AR regulation in human airway cells. We have employed a bronchoscopy model to examine inflammation- and beta-agonist-induced alterations in human bronchial epithelial cell beta 2-AR density and responsiveness. Allergic asthmatic subjects participated in 2-day protocols examining airways before and 24 h after segmental antigen challenge (SAC) with ragweed. To assess the effect of acute beta-

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23

Eff, Aprilita Rina Yanti. "INCIDENCE OF HYPERTENSION IN ASTHMA PATIENTS WHO TREATED WITH BETA-2 AGONISTS BRONCHODILATORS." International Journal of Pharmacy and Pharmaceutical Sciences 9, no. 4 (2017): 181. http://dx.doi.org/10.22159/ijpps.2017v9i4.17013.

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Objective: To determine the prevalence of hypertension in hospitalized patients with asthma who were treated with beta-2 agonists. To evaluate the correlation between the duration of the use of beta-2 agonist with the incidence of hypertension.Methods: This research is a descriptive epidemiological, observational cross-sectional and retrospective study design. The study population was all adult asthma patients (age ≥ 25) without a concomitant diseases such as hypertension or metabolic syndrome treated with β2 agonists as a bronchodilator and underwent hospitalized in January 2015-December 2015

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24

&NA;. "Beta agonist-related tremorogenic effects." Reactions Weekly &NA;, no. 300 (1990): 1. http://dx.doi.org/10.2165/00128415-199003000-00001.

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25

SCHNAPF, BRUCE M., and MARIA L. SANTEIRO. "Beta-agonist inhaler causing hallucinations." Pediatric Emergency Care 10, no. 2 (1994): 87–88. http://dx.doi.org/10.1097/00006565-199404000-00006.

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26

Wong, L. B., I. F. Miller, and D. B. Yeates. "Stimulation of ciliary beat frequency by autonomic agonists: in vivo." Journal of Applied Physiology 65, no. 2 (1988): 971–81. http://dx.doi.org/10.1152/jappl.1988.65.2.971.

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beta 2-Adrenergic bronchodilator and muscarinic cholinergic bronchoconstrictor agonists both stimulate ciliary activity in vitro. To test the hypothesis that increases in autonomic activity would result in increases in ciliary beat frequency (CBF) in vivo, a correlation analysis heterodyne laser light-scattering system was developed and validated to measure the stimulating effects of sympathomimetic and parasympathomimetic agonists on tracheal CBF in intact, anesthetized beagles. The mean baseline CBF from 42 studies of 274 measurements in 9 (5 male and 4 female) adult beagles was 6.6 +/- 1.1

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27

Blaak, E. E., M. A. van Baak, K. P. Kempen, and W. H. Saris. "Role of alpha- and beta-adrenoceptors in sympathetically mediated thermogenesis." American Journal of Physiology-Endocrinology and Metabolism 264, no. 1 (1993): E11—E17. http://dx.doi.org/10.1152/ajpendo.1993.264.1.e11.

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This study was intended to investigate the role of alpha- and beta-adrenoceptor populations in the sympathetically mediated thermogenesis in healthy lean males. In the first study, the beta 1-, beta 2-, and beta 3-agonist isoprenaline was infused in increasing doses with and without simultaneous infusion of the beta 1-blocker atenolol (Iso and Iso+AT, respectively). There was an increase in whole body energy expenditure (EE) after infusing Iso+AT (P < 0.001) and an almost twofold higher increase after infusion of Iso only (P < 0.001). Stimulation of the beta 2-adrenoceptors by a specific

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28

Tetens, V., G. Lykkeboe, and N. J. Christensen. "Potency of adrenaline and noradrenaline for beta-adrenergic proton extrusion from red cells of rainbow trout, Salmo gairdneri." Journal of Experimental Biology 134, no. 1 (1988): 267–80. http://dx.doi.org/10.1242/jeb.134.1.267.

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The red cell adrenoceptor affinity for the unspecific agonists adrenaline and noradrenaline and the specific beta-agonist isoprenaline was studied in vitro on whole blood of rainbow trout, Salmo gairdneri at 15 degrees C. The erythrocytic adrenoceptors could be pharmacologically characterized as beta-receptors of the ‘noradrenaline’-type (beta 1-type), with an order of potency of isoprenaline greater than noradrenaline much greater than adrenaline. The adrenoceptor affinities, expressed as agonist concentrations for 50% response (EC50), were 1.3 X 10(−8) and 7.6 X 10(−7) mol l-1 for noradrenal

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29

Aprigliano, O., V. O. Rybin, E. Pak, R. B. Robinson, and S. F. Steinberg. "beta 1-and beta 2-adrenergic receptors exhibit differing susceptibility to muscarinic accentuated antagonism." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 6 (1997): H2726—H2735. http://dx.doi.org/10.1152/ajpheart.1997.272.6.h2726.

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Neonatal rat ventricular myocytes express both beta 1-and beta 2-adrenergic receptors linked to enhanced intracellular adenosine 3',5'-cyclic monophosphate (cAMP) accumulation and the modulation of contractile function. This study tests the hypothesis that muscarinic agonists act via distinct mechanisms to interfere with beta 1-and beta 2-adrenergic receptor actions. The beta 2-selective agonist zinterol (10(-7) M) elicits approximately a fourfold increase in cAMP accumulation, which is mimicked, both in magnitude and kinetics, by 10(-9) M of the mixed beta 1-receptor agonist/beta 2-receptor a

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30

Desai, Rooma, Dirk Ruesch та Stuart A. Forman. "γ-Amino Butyric Acid Type A Receptor Mutations at β2N265 Alter Etomidate Efficacy While Preserving Basal and Agonist-dependent Activity". Anesthesiology 111, № 4 (2009): 774–84. http://dx.doi.org/10.1097/aln.0b013e3181b55fae.

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Background Etomidate acts at gamma-Aminobutyric acid type A (GABAA) receptors containing beta2 or beta3, but not beta1 subunits. Mutations at beta residue 265 (Ser in beta1; Asn in beta2 or beta3) profoundly affect etomidate sensitivity. Whether these mutations alter etomidate binding remains uncertain. Methods Heterologously expressed alpha1beta2gamma2L GABAA receptors and receptors with beta2(N265S) or beta2(N265M) mutations were studied electrophysiologically in both Xenopus oocytes and HEK293 cells. Experiments quantified the impact of beta2N265 mutations or substituting beta1 for beta2 on

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31

Grider, J. R., and G. M. Makhlouf. "Identification of opioid receptors on gastric muscle cells by selective receptor protection." American Journal of Physiology-Gastrointestinal and Liver Physiology 260, no. 1 (1991): G103—G107. http://dx.doi.org/10.1152/ajpgi.1991.260.1.g103.

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Opioid receptors on isolated gastric smooth muscle cells were characterized pharmacologically by a technique in which synthetic selective opioid agonists and antagonists were used to protect and thus enrich a specific receptor type while all other receptors were inactivated by N-ethylamaleimide. Treatment of the cells with the selective mu-receptor agonist DAGO or antagonist CTAP preserved only the response to DAGO; treatment with the selective delta-receptor agonist DPDPE or antagonist naltrindole preserved only the response to DPPE; and treatment with the selective kappa-receptor agonist U50

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Zink, S., P. Rosen, and H. Lemoine. "Micro- and macrovascular endothelial cells in beta-adrenergic regulation of transendothelial permeability." American Journal of Physiology-Cell Physiology 269, no. 5 (1995): C1209—C1218. http://dx.doi.org/10.1152/ajpcell.1995.269.5.c1209.

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Barrier function of endothelial cells (EC) was modulated using beta-adrenergic agonists, e.g., isoproterenol (ISO) and formoterol (FOR). To get a direct comparison between EC from different vascular sources, we isolated EC from aorta (BAEC) and retina (BREC) of the same calf. For permeability studies, EC were cultured on polycarbonate filters. At confluency, transendothelial exchange of the diffusion marker fluorescein isothiocyanate-dextran was determined. Microvascular retinal EC monolayers are half as permeable as monolayers from macrovascular BAEC. When EC are stimulated with beta-adrenerg

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Bondy, B., M. Ackenheil, G. Laakmann, and H. T. Munz. "Influnce of the beta-adrenergic agonist clenbuterol on plasma catecholamines and lymphocyte beta-receptors." Psychiatry and Psychobiology 1, no. 3 (1986): 234–36. http://dx.doi.org/10.1017/s0767399x00000080.

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SummaryThe influence of subchronic application of the β-adrenergic agonist clenbuterol on plasma norepinephrine (NE), epinephrine (E) and β-receptors on lymphocytes was investigated in 8 male, healthy volunteers. Treatment with clenbuterol (0.04 mg/day) for 6 days induced significant reduction of β-receptor specific binding in 7 of the 8 subjects with a mean decrease of 40% (p < 0.01) with no changes in affinity. Concomitantly an increase in the plasma NE concentration was observed (mean 50%, p < 0.01), but no significant overall alteration of E concentration. Our results suggest that β-

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34

Khimenko, P. L., T. M. Moore, L. W. Hill, et al. "Adenosine A2 receptors reverse ischemia-reperfusion lung injury independent of beta-receptors." Journal of Applied Physiology 78, no. 3 (1995): 990–96. http://dx.doi.org/10.1152/jappl.1995.78.3.990.

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To evaluate the adenosine systems ability to reverse the endothelial damage produced by ischemia and reperfusion (I/R), we studied several different selective adenosine-receptor agonists and antagonists, a protein kinase A inhibitor, and a beta-adrenoreceptor antagonist in isolated buffer-perfused rat lungs. I/R (45 min/105 min) produced a sixfold increase in endothelial permeability as measured by the capillary filtration coefficient. Both a selective A2-receptor agonist (CGS-21680, 300 nM) and a beta-receptor agonist (isoproterenol, 10 microM) reversed the increased microvascular permeabilit

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35

Takayanagi, Issei. "Agonist site and antagonist site for beta-adrenergic partial agonist." Japanese Journal of Pharmacology 39 (1985): 36. http://dx.doi.org/10.1016/s0021-5198(19)63271-3.

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Lewis, C. A., Z. Ahmed, and D. S. Faber. "A characterization of glycinergic receptors present in cultured rat medullary neurons." Journal of Neurophysiology 66, no. 4 (1991): 1291–303. http://dx.doi.org/10.1152/jn.1991.66.4.1291.

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1. Whole-cell current responses to bath application of glycine, beta-alanine, and taurine were studied in medullary neurons cultured from embryonic rats. 2. Two current components were seen in the responses to bath application of agonist, one component that desensitized and another that did not. 3. The two current components have different dose-response characteristics, with the nondesensitizing component being activated more effectively at lower concentrations than the desensitizing component and also reaching its peak at lower concentrations. The agonist concentrations producing half-maximal

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Paul, A., M. Mergey, D. Veissiere, et al. "Regulation of secretion in cultured tracheal serous cells by protein kinases A and C." American Journal of Physiology-Lung Cellular and Molecular Physiology 261, no. 2 (1991): L172—L177. http://dx.doi.org/10.1152/ajplung.1991.261.2.l172.

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We recently reported that cultured gland serous cells release chondroitin sulfate proteoglycans (CSPGs) in response to beta-adrenergic agonists. In this study, we analyzed this regulatory pathway and other cellular mechanisms responsible for CSPG secretion. We show the following. 1) Isoproterenol increased CSPG secretion in a concentration-dependent manner, with maximal stimulation (50%) obtained at 10(-5) M; at this concentration, the beta-agonist also stimulated protein kinase A (PKA) by 50%, whereas it increased cellular adenosine 3',5'-cyclic monophosphate (cAMP) content by 300%. 2) Phenyl

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Tamaoki, J., F. Yamauchi, A. Chiyotani, I. Yamawaki, S. Takeuchi, and K. Konno. "Atypical beta-adrenoceptor- (beta 3-adrenoceptor) mediated relaxation of canine isolated bronchial smooth muscle." Journal of Applied Physiology 74, no. 1 (1993): 297–302. http://dx.doi.org/10.1152/jappl.1993.74.1.297.

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To determine whether atypical beta-adrenoceptors (beta 3-adrenoceptors) exist in the airway smooth muscle, we studied isolated bronchial segments from dogs under isometric conditions in vitro. Addition of beta-adrenoceptor agonists produced a concentration-dependent relaxation of tissues precontracted with 10(-5) M acetylcholine, rank-order potency being isoproterenol (1) > or = salbutamol (0.95) > or = BRL 37344, a beta 3-selective adrenoceptor agonist (0.83) > norepinephrine (0.10). Under the condition that alpha- and beta 1-adrenoceptors had been blocked, the relaxant response to s

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39

Janeiro, Sérgio, Suzane Ribeiro, Daniel Trabulo, Susana Marques, and Ermelinda Pedroso. "BETA-2 AGONIST AND LACTIC ACIDOSIS." European Journal of Internal Medicine 22 (October 2011): S42. http://dx.doi.org/10.1016/s0953-6205(11)60173-8.

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40

Williams, Dennis M. "Beta Agonist Therapy: MDI or Nebulizer?" American Pharmacy 31, no. 9 (1991): 36–38. http://dx.doi.org/10.1016/s0160-3450(16)33839-9.

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41

Potter, Paul. "Trends in Beta-2 Agonist Therapy." Allergy & Clinical Immunology International - Journal of the World Allergy Organization 19, no. 4 (2007): 155–58. http://dx.doi.org/10.1027/0838-1925.19.4.155.

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42

&NA;. "Comments on the beta agonist controversy." Inpharma Weekly &NA;, no. 776 (1991): 4–5. http://dx.doi.org/10.2165/00128413-199107760-00008.

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43

Crane, J., N. Pearce, C. Burgess, and R. Beasley. "Asthma and the beta agonist debate." Thorax 50, Suppl 1 (1995): S5—S10. http://dx.doi.org/10.1136/thx.50.suppl_1.s5.

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44

Richter, B. "Asthma and regular beta agonist treatment." BMJ 303, no. 6803 (1991): 648. http://dx.doi.org/10.1136/bmj.303.6803.648-b.

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45

RUFFIN;, D., and T. W. HARRISON. "Beta agonist dose reduction in asthma." Thorax 54, no. 9 (1999): 861. http://dx.doi.org/10.1136/thx.54.9.861.

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46

Bishop, Michael J. "Beta Agonist Delivery and the Outpatient." Chest 96, no. 6 (1989): 1219–20. http://dx.doi.org/10.1378/chest.96.6.1219b.

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47

Brooks, D. P., L. Share, and J. T. Crofton. "Central adrenergic mechanisms in hemorrhage-induced vasopressin secretion." American Journal of Physiology-Heart and Circulatory Physiology 251, no. 6 (1986): H1158—H1162. http://dx.doi.org/10.1152/ajpheart.1986.251.6.h1158.

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The effect of central administration of specific adrenergic agonists and antagonists on hemorrhage-induced vasopressin secretion was studied in conscious rats. The intracerebroventricular (icv) injection of the alpha 2-antagonist yohimbine, the alpha 1-antagonist corynanthine, or the beta-agonist isoproterenol failed to alter the vasopressin or blood pressure responses to two sequential 10% reductions in blood volume. Administration of the beta-antagonist propranolol, however, resulted in a significant attenuation of the vasopressin response to hemorrhage, with little effect on the blood press

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48

Asano, K., Y. Suzuki, T. Shiomi, et al. "Airway responsiveness to beta-agonist and beta2-adrenoceptor gene polymorphisms." Journal of Allergy and Clinical Immunology 111, no. 2 (2003): S269. http://dx.doi.org/10.1016/s0091-6749(03)80964-8.

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49

Sears, Malcolm R. "Epidemiological Trends in Asthma." Canadian Respiratory Journal 3, no. 4 (1996): 261–68. http://dx.doi.org/10.1155/1996/410215.

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Many markers of asthma morbidity have shown substantial increases over the past two decades, including family physician visits, use of anti-asthma medications, emergency room visits and hospital admissions. The reported prevalence of diagnosed asthma and of wheezing has increased, especially in children, with accompanying evidence of increased atopy and increased airway responsiveness. Allergen exposure and parental smoking are significant risk factors for childhood wheezing, whereas the influence of outdoor air pollution is uncertain. Increasing use of beta-agonist treatment, which appears to

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50

Quan, N., L. Xin, A. L. Ungar, and C. M. Blatteis. "Preoptic norepinephrine-induced hypothermia is mediated by alpha 2-adrenoceptors." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 262, no. 3 (1992): R407—R411. http://dx.doi.org/10.1152/ajpregu.1992.262.3.r407.

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We have shown previously that norepinephrine (NE) microdialyzed into the preoptic area of conscious guinea pigs evokes a fall in core temperature (Tco) that is mediated by a reduction in metabolic rate. To identify the adrenoceptor subtype(s) involved in this effect, we microdialyzed intrapreoptically various adrenergic agonists or antagonists singly or in combinations. Tco and ear skin temperatures of the animals were monitored throughout the experiments. alpha 1-, beta-, beta 1-, and beta 2-agonists and antagonists did not induce significant Tco changes. Although the alpha 2-antagonists yohi

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