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Journal articles on the topic 'Beta agonists'

Author: Grafiati

Published: 4 June 2021

Last updated: 26 July 2025

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1

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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2

&NA;. "Beta agonists." Reactions Weekly &NA;, no. 578 (1995): 5. http://dx.doi.org/10.2165/00128415-199505780-00013.

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&NA;. "Beta agonists." Reactions Weekly &NA;, no. 430 (1992): 6. http://dx.doi.org/10.2165/00128415-199204300-00023.

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&NA;. "Beta agonists." Reactions Weekly &NA;, no. 414 (1992): 5. http://dx.doi.org/10.2165/00128415-199204140-00012.

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&NA;. "Beta agonists." Reactions Weekly &NA;, no. 312 (1990): 4. http://dx.doi.org/10.2165/00128415-199003120-00012.

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&NA;. "Beta agonists." Reactions Weekly &NA;, no. 487 (1994): 5. http://dx.doi.org/10.2165/00128415-199404870-00017.

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&NA;. "Beta agonists." Reactions Weekly &NA;, no. 500 (1994): 5. http://dx.doi.org/10.2165/00128415-199405000-00014.

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8

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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9

Oscanoa, T. J. "Seguridad de los beta 2 agonistas (?2a) en asma bronquial." Revista de la Facultad de Ciencias Médicas de Córdoba 71, no. 1 (2014): 43–53. http://dx.doi.org/10.31053/1853.0605.v71.n1.8426.

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ResumenLos broncodilatadores beta 2 agonistas (?2A) forman parte muy importante en el farmacoterapia del asma bronquial, una enfermedad que avanza en el mundo de manera epidémica. Los ?2A son prescritos a millones de personas en el mundo, por consiguiente los aspectos de seguridad son de interés público. Los broncodilatadores ?2A de acción corta (Short-Acting ?2 Agonists o SABA) como salbutamol inhalatorio, según las evidencias actuales, confirman su seguridad en su uso como fármaco de rescate o a demanda. Los broncodilatadores ?2A de acción prolongada (Long-Acting ?2 Agonists o LABA) se utili

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10

Feldman, R. D., G. W. Hunninghake, and W. L. McArdle. "Beta-adrenergic-receptor-mediated suppression of interleukin 2 receptors in human lymphocytes." Journal of Immunology 139, no. 10 (1987): 3355–59. http://dx.doi.org/10.4049/jimmunol.139.10.3355.

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Abstract Adrenergic receptor agonists are known to attenuate the proliferative response of human lymphocytes after activation; however, their mechanism of action is unknown. Since expression of interleukin 2 (IL-2) receptors is a prerequisite for proliferation, the effect of beta-adrenergic receptor agonists on lymphocyte IL-2 receptors was studied on both mitogen-stimulated lymphocytes and IL-2-dependent T lymphocyte cell lines. In both cell types the beta-adrenergic receptor agonist isoproterenol blocked the expression of IL-2 receptors, as determined with the IL-2 receptor anti-TAC antibody

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11

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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12

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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13

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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14

Brown, PH, J. Lenney, S. Armstrong, AC Ning, and GK Crompton. "Breath-actuated inhalers in chronic asthma: comparison of Diskhaler and Turbohaler for delivery of beta-agonists." European Respiratory Journal 5, no. 9 (1992): 1143–45. http://dx.doi.org/10.1183/09031936.93.05091143.

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An open, randomized, cross-over study was performed to compare the efficacy and acceptability of two breath-actuated inhalers, the Turbohaler (T) and Diskhaler (D), for delivery of beta-agonists. Thirty six adults with chronic asthma requiring beta-agonists four times daily were treated with terbutaline 500 micrograms via T and salbutamol 400 micrograms via D four times daily, each period lasting four weeks. Additional bronchodilator via pressurized aerosol was permitted as required. Peak expiratory flow (PEF) was recorded in the morning (before and after beta-agonist) and in the evening. The

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15

Barisione, Giovanni, Michele Baroffio, Emanuele Crimi, and Vito Brusasco. "Beta-Adrenergic Agonists." Pharmaceuticals 3, no. 4 (2010): 1016–44. http://dx.doi.org/10.3390/ph3041016.

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16

BOYLE, JEFFREY G. "Beta-Adrenergic Agonists." Clinical Obstetrics and Gynecology 38, no. 4 (1995): 688–96. http://dx.doi.org/10.1097/00003081-199538040-00003.

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17

Pelton Sterling, Lisa. "Beta Adrenergic Agonists." AACN Clinical Issues: Advanced Practice in Acute and Critical Care 6, no. 2 (1995): 271–78. http://dx.doi.org/10.1097/00044067-199505000-00010.

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18

Hoisington, Lisa M. "Inhaled Beta-Agonists." Journal of Cardiopulmonary Rehabilitation 12, no. 4 (1992): 233–36. http://dx.doi.org/10.1097/00008483-199207000-00001.

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19

Fernandez, Enrique. "Beta-Adrenergic Agonists." Seminars in Respiratory and Critical Care Medicine 8, no. 04 (1987): 353–65. http://dx.doi.org/10.1055/s-2007-1012675.

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20

Skorodin, Morton S. "Beta-adrenergic Agonists." Chest 103, no. 5 (1993): 1587–90. http://dx.doi.org/10.1378/chest.103.5.1587.

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21

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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22

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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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

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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25

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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26

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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27

Khusial, Rishi Jayant, Jacob K. Sont, Omar S. Usmani, et al. "The Effect of Inhaled Beta-2 Agonists on Heart Rate in Patients With Asthma: Sensor-Based Observational Study." JMIR Cardio 8 (December 11, 2024): e56848. https://doi.org/10.2196/56848.

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Background Beta-2 agonists play an important role in the management of asthma. Inhaled long-acting beta-2 agonists (LABAs) and short-acting beta-2 agonists (SABAs) cause bronchodilation by stimulating adrenoceptors. These receptors are also present in cardiac cells and, as a side effect, could also be stimulated by inhaled beta-2 agonists. Objective This study aims to assess the effect of beta-2 agonists on heart rate (HR). Methods The data were retrieved from an observational study, the myAirCoach Quantification Campaign. Beta-2 agonist use was registered by self-reported monthly questionnair

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28

Tattersfield, A. E., and P. Wilding. "Beta agonists and ventilation." Thorax 48, no. 9 (1993): 877–78. http://dx.doi.org/10.1136/thx.48.9.877.

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29

Spiegler, Peter. "Beta-agonists for ARDS." Clinical Pulmonary Medicine 19, no. 1 (2012): 48–49. http://dx.doi.org/10.1097/cpm.0b013e31823df7b5.

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30

&NA;. "Comparing inhaled beta agonists." Inpharma Weekly &NA;, no. 819 (1992): 20. http://dx.doi.org/10.2165/00128413-199208190-00059.

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&NA;. "Beta agonists in asthma." Inpharma Weekly &NA;, no. 830 (1992): 6. http://dx.doi.org/10.2165/00128413-199208300-00009.

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32

ROLFSMITH, S. "BETA AGONISTS AND POTASSIUM." Lancet 325, no. 8442 (1985): 1394–95. http://dx.doi.org/10.1016/s0140-6736(85)91822-7.

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33

Taylor, D. Robin, and Malcolm R. Sears. "Regular Beta-Adrenergic Agonists." Chest 106, no. 2 (1994): 552–59. http://dx.doi.org/10.1378/chest.106.2.552.

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34

Bousquet-Melou, A., J. Galitzky, C. Carpene, M. Lafontan, and M. Berlan. "beta-Adrenergic control of lipolysis in primate white fat cells: a comparative study with nonprimate mammals." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 267, no. 1 (1994): R115—R123. http://dx.doi.org/10.1152/ajpregu.1994.267.1.r115.

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The beta-adrenoceptor subtypes involved in the control of lipolysis in white fat cells of rat, dog, marmoset (Callithrix jacchus), baboon (Papio papio), macaque (Macaca fascicularis), and human were compared. In all species [3H]CGP-12177 binding (up to 3 nM) indicated the existence of a homogeneous population of binding sites in fat cell membranes, and competition studies showed that beta 1- and beta 2-adrenoceptors were present. Selective beta 1 or beta 2-adrenoceptor agonists induced lipolysis. The efficiencies of isoproterenol and norepinephrine were similar. The use of selective beta 3-adr

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35

Zhang, L., R. T. Jensen, and P. N. Maton. "Characterization of beta-adrenoreceptors on smooth muscle cells from guinea pig stomach." American Journal of Physiology-Gastrointestinal and Liver Physiology 259, no. 3 (1990): G436—G442. http://dx.doi.org/10.1152/ajpgi.1990.259.3.g436.

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To characterize the beta-adrenergic receptors on guinea pig gastric smooth muscle cells, we examined the effects of beta-adrenergic agonists and antagonists on biological activity, cellular adenosine 3',5'-cyclic monophosphate (cAMP), and radioligand binding. Adrenergic agonists, isoproterenol (ISO), epinephrine (EPI), and norepinephrine (NE), inhibited carbachol-stimulated contraction of muscle cells, with relative potencies (IC50S) of ISO (0.1 microM) greater than EPI (1.4 microM) greater than NE (11 microM). Each agonist increased cellular cAMP, with relative potencies (IC50S) of ISO (0.5 m

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36

Le, Kang, Wendy K. Steagall, Mario Stylianou, et al. "Effect of beta-agonists on LAM progression and treatment." Proceedings of the National Academy of Sciences 115, no. 5 (2018): E944—E953. http://dx.doi.org/10.1073/pnas.1719960115.

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Lymphangioleiomyomatosis (LAM), a rare disease of women, is associated with cystic lung destruction resulting from the proliferation of abnormal smooth muscle-like LAM cells with mutations in the tuberous sclerosis complex (TSC) genes TSC1 and/or TSC2. The mutant genes and encoded proteins are responsible for activation of the mechanistic target of rapamycin (mTOR), which is inhibited by sirolimus (rapamycin), a drug used to treat LAM. Patients who have LAM may also be treated with bronchodilators for asthma-like symptoms due to LAM. We observed stabilization of forced expiratory volume in 1 s

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37

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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38

Pascali, Francesco D., Michael Ippolito, Emily Wolfe, et al. "LBMON186 Beta-agonist Profiling Reveals Novel Biased Signaling Phenotypes For The Beta 2-adrenergic Receptor With Implications In The Treatment Of Asthma." Journal of the Endocrine Society 6, Supplement_1 (2022): A587—A588. http://dx.doi.org/10.1210/jendso/bvac150.1217.

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Abstract Asthma involves chronic airway inflammation and airway smooth muscle (ASM) cell contraction. Treatment include agonists of the beta 2-AR, a GPCR that induces the Gs/cAMP pathway leading to ASM relaxation. These agonists can also promote severe side effects which have been correlated with beta-arrestins (barr) activation. Therefore, biased ligands selective for the Gs/cAMP pathway over the barr-induced side effects should be beneficial. To test this, we have used high-throughput screening to identify Gs-biased agonists. The initial lead candidates were further analyzed for their abilit

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39

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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40

Carpéné, C., E. Chalaux, M. Lizarbe та ін. "β 3-adrenergic receptors are responsible for the adrenergic inhibition of insulin-stimulated glucose transport in rat adipocytes". Biochemical Journal 296, № 1 (1993): 99–105. http://dx.doi.org/10.1042/bj2960099.

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The inhibition of insulin-stimulated glucose transport by isoprenaline, a mixed beta-adrenergic-receptor (AR) agonist, is well documented in rat adipocytes. Since it has been described that rat adipocytes possess not only beta 1- and beta 2- but also beta 3-ARs, the influence of various subtype-selective beta-AR agonists and antagonists on 2-deoxyglucose (2-DG) transport was assessed in order to characterize the beta-AR subtype involved in the adrenergic counter-regulation of the insulin effect. The stimulation of 2-DG transport by insulin was counteracted, in a dose-dependent manner, by all t

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Piiper, A., D. Stryjek-Kaminska, R. Klengel, and S. Zeuzem. "CCK, carbachol, and bombesin activate distinct PLC-beta isoenzymes via Gq/11 in rat pancreatic acinar membranes." American Journal of Physiology-Gastrointestinal and Liver Physiology 272, no. 1 (1997): G135—G140. http://dx.doi.org/10.1152/ajpgi.1997.272.1.g135.

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Four different isoforms of phospholipase C-beta (PLC-beta 1-4) have been discovered, raising the important question of whether a distinct receptor activates a single PLC-beta isoenzyme or a subset of PLC-beta isoenzymes. The present study was designed to investigate activation of PLC-beta isoenzymes by three different PLC-activating agonists that bind to different receptor entities, i.e., cholecystokinin octapeptide (CCK-8), bombesin, and carbachol in rat pancreatic acinar membranes. PLC activity was measured using exogenous [3H]phosphatidylinositol 4,5-bisphosphate as substrate. Western blot

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42

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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43

Dasta, Joseph F., David A. Kuhl, Olakunbi A. Agiri, and Laurie S. Mauro. "Beta-Agonists in the Treatment of Acute Exacerbation of Chronic Obstructive Pulmonary Disease." Annals of Pharmacotherapy 28, no. 12 (1994): 1379–88. http://dx.doi.org/10.1177/106002809402801209.

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OBJECTIVE: To critically evaluate the following issues regarding the use of beta-agonists in the treatment of acute exacerbations of chronic obstructive pulmonary disease (COPD): (1) optimal dose, (2) use of nebulizer (NEB) versus metered-dose inhaler-spacer devices (MDISs), (3) comparison with anticholinergic agents, and (4) use in mechanically ventilated patients. The patient populations addressed are limited primarily to emergency department (ED) and intensive care/acute care settings. DATA SOURCES: English-language journal articles published between 1977 and 1993. STUDY SELECTION: Nine stu

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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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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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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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Chu, T. C., and O. A. Candia. "Role of alpha 1- and alpha 2-adrenergic receptors in Cl- transport across frog corneal epithelium." American Journal of Physiology-Cell Physiology 255, no. 6 (1988): C724—C730. http://dx.doi.org/10.1152/ajpcell.1988.255.6.c724.

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Norepinephrine, 10(-6) M, reduced Cl- transport by 26% in 75% of isolated frog corneal epithelia. This inhibition was not previously reported. Since beta-adrenergic agonists are known to only stimulate Cl- transport, the action of specific alpha 1- and alpha 2-agonists on Cl- transport and electrical parameters was investigated. Phenylephrine, an alpha 1-agonist always stimulated the Cl(-)-dependent short-circuit current (Isc), but less than the beta-agonists. UK-14,304-18 (UK), a selective alpha 2-agonist, reduced both the Isc (by 31% at 10(-5) M) and the stroma-to-tear unidirectional Cl- flu

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Gómez, Constanza, Gonzalo Alarcón, and Lorena Cifuentes. "Beta-2 agonists for the treatment of bronchiolitis." Medwave 20, no. 08 (2020): e7947-e7947. http://dx.doi.org/10.5867/medwave.2020.08.7947.

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Frielle, T., M. G. Caron, and R. J. Lefkowitz. "Properties of the beta 1- and beta 2-adrenergic receptor subtypes revealed by molecular cloning." Clinical Chemistry 35, no. 5 (1989): 721–25. http://dx.doi.org/10.1093/clinchem/35.5.721.

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Abstract The beta 1- and beta 2-adrenergic receptor subtypes are biochemically and functionally similar, because both receptors mediate the catecholamine-dependent activation of adenylate cyclase through the GTP-binding protein, Gs. Pharmacologically, the two receptors can be distinguished on the basis of their relative affinities for the agonists epinephrine and norepinephrine as well as their affinities for several selective antagonists. The primary structures of the human beta 1- and beta 2-adrenergic receptors have recently been deduced from the cloning of their genes and (or) cDNAs, revea

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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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