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Journal articles on the topic 'An agonist of beta-blockers'

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Published: 7 June 2025

Last updated: 2 August 2025

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1

Fitzgerald, J. D. "Do partial agonist beta-blockers have improved clinical utility?" Cardiovascular Drugs and Therapy 7, no. 3 (1993): 303–10. http://dx.doi.org/10.1007/bf00880153.

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2

Yoshikawa, Tsutomu. "Inverse Agonism of Beta-Blockers." Journal of Cardiac Failure 11, no. 9 (2005): S244. http://dx.doi.org/10.1016/j.cardfail.2005.08.045.

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3

Van, An Thi Minh, and Nawaid Ahmad. "Selective Beta-Blockers on Chronic Obstructive Pulmonary Disease: A Literature Review." Respiratory Science 4, no. 3 (2024): 180–96. http://dx.doi.org/10.36497/respirsci.v4i3.131.

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Chronic obstructive pulmonary disease (COPD) and cardiovascular disease (CVD) are usually coexisting. While beta-blockers are the indispensable management of an array of cardiovascular diseases, inhaled beta-receptor agonists are the central treatment for COPD patients. This review aims to assess the effect of beta-blockers on exacerbation rate, mortality, and quality of life among the COPD population. After the search on Cochrane Library, Pubmed, and Scopus, 15 relevant full-text articles published between 2012 and 2022 were included. We compared selective beta-blockers versus either non-user

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4

London, Martin J. "Beta blockers and alpha2 agonists for cardioprotection." Best Practice & Research Clinical Anaesthesiology 22, no. 1 (2008): 95–110. http://dx.doi.org/10.1016/j.bpa.2007.09.008.

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5

TURABI, AFTAB, Naseer Baluch, S. SAUD HASAN, Mehar Ali, and AHMED DANYAL. "ADRENALINE & ITS ANTAGONIST." Professional Medical Journal 12, no. 04 (2005): 420–25. http://dx.doi.org/10.29309/tpmj/2005.12.04.5093.

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Objective: This research work deals with the mechanism involved in determining the therapeuticpotential of adrenaline and its blockers in gastrointestinal motility. Method: The classical method of Craig & Clark wasused for obtaining the longitudinal and circular muscles strip of rabbit intestine for in-vitro studies. Each muscle stripseparately was subjected to the effect of adrenaline and its blockers. The results were recorded on polygraphapparatus. Results: The effects were recorded in vice versa fashion i.e. agonist v/s antagonist and antagonist v/sagonist on each muscle strip separate

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6

Gough, N. R. "-Blockers: Both Antagonist and Agonist." Science Signaling 1, no. 39 (2008): ec336-ec336. http://dx.doi.org/10.1126/scisignal.139ec336.

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7

Thor, Doreen, Angela Schulz, Thomas Hermsdorf, and Torsten Schöneberg. "Generation of an agonistic binding site for blockers of the M3 muscarinic acetylcholine receptor." Biochemical Journal 412, no. 1 (2008): 103–12. http://dx.doi.org/10.1042/bj20071366.

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GPCRs (G-protein-coupled receptors) exist in a spontaneous equilibrium between active and inactive conformations that are stabilized by agonists and inverse agonists respectively. Because ligand binding of agonists and inverse agonists often occurs in a competitive manner, one can assume an overlap between both binding sites. Only a few studies report mutations in GPCRs that convert receptor blockers into agonists by unknown mechanisms. Taking advantage of a genetically modified yeast strain, we screened libraries of mutant M3Rs {M3 mAChRs [muscarinic ACh (acetylcholine) receptors)]} and ident

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8

Channer, KS, MA James, T. MacConnell, and JR Rees. "Beta-adrenoceptor blockers in atrial fibrillation: the importance of partial agonist activity [see comments]." British Journal of Clinical Pharmacology 37, no. 1 (1994): 53–57. http://dx.doi.org/10.1111/j.1365-2125.1994.tb04238.x.

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9

Herxheimer, A. "Beta-adrenoceptor blockers in atrial fibrillation: the importance of partial agonist activity [letter; comment]." British Journal of Clinical Pharmacology 37, no. 6 (1994): 613–76. http://dx.doi.org/10.1111/j.1365-2125.1994.tb04313.x.

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10

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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11

Kovačević, Dragan, and Sanja Kovačević. "Significance of beta-blocker dose titration in heart failure." Galenika Medical Journal 1, no. 4 (2022): 53–58. http://dx.doi.org/10.5937/galmed2204055k.

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Heart failure is a clinical syndrome, characterized by the inability of the heart to pump an adequate amount of blood according to the needs of the organs and tissues, at rest and during exertion, despite normal blood flow to the heart. Treatment includes hygienic and dietary measures, pharmacological treatment, installation of an appropriate device, surgical treatment and heart transplantation. Indispensable groups of drugs that reduce mortality in the treatment of this disease are beta-blockers, angiotensin-converting enzyme inhibitors (ACE inhibitors)/angiotensin receptor neprilysin inhibit

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12

Anderson, William, Philip Short, Rose Ross, and Brian J. Lipworth. "Bisoprolol versus celiprolol on dynamic hyperinflation, cardiopulmonary exercise and domiciliary safety in COPD: a single-centre, randomised, crossover study." BMJ Open Respiratory Research 10, no. 1 (2023): e001670. http://dx.doi.org/10.1136/bmjresp-2023-001670.

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BackgroundChronic obstructive pulmonary disease (COPD) is frequently associated with cardiovascular disease. The utility of beta-blockers for treating patients with COPD may be beneficial, but their safety remains uncertain, including worsening of dynamic hyperinflation (DH) during exercise. We hypothesised that among cardioselective beta-blockers celiprolol, due to its partial beta-2 agonist activity, may be safer than bisoprolol on exercise DH.MethodsWe measured isotime inspiratory capacity (IC) during cycle endurance testing in eleven moderate-severe COPD subjects, alongside other non-invas

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13

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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14

Wallnofer, A., C. Cauvin, T. W. Lategan, and U. T. Ruegg. "Differential blockade of agonist- and depolarization-induced 45Ca2+ influx in smooth muscle cells." American Journal of Physiology-Cell Physiology 257, no. 4 (1989): C607—C611. http://dx.doi.org/10.1152/ajpcell.1989.257.4.c607.

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ATP stimulated 45Ca2+ influx in rat aortic smooth muscle cells in a concentration-dependent manner (EC50 = 3.6 +/- 0.5 X 10(-7) M). ADP and GTP were less effective than ATP in stimulating 45Ca2+ influx; AMP was weakly active and the adenosine agonist 5'-(N-ethyl-carboxamido)-adenosine (NECA) had no effect. ATP gamma S was about equieffective with ATP, whereas alpha,beta-methylene-ATP (APCPP) did not induce 45Ca2+ influx. Stimulation of 45Ca2+ influx by ATP was not abolished by the dihydropyridine Ca2+ channel antagonist darodipine (PY 108-068), which completely blocked depolarization-induced 4

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15

Mohamed Saleem TS, Sreeja N, Kiran Karthik J, and Bhanu Sree K. "Cost effectiveness analysis of anti-hypertensive drugs used for chronic kidney disease patients." International Journal of Research in Pharmaceutical Sciences 10, no. 4 (2019): 2820–25. http://dx.doi.org/10.26452/ijrps.v10i4.1553.

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Cost effectiveness analysis branch of pharmacoeconomics is a technique used to aid in decision making between alternatives. A prospective observational study would be conducted in the nephrology department at O.P, Patients with CKD with hypertension, with or deprived of diabetes are included in the study. Patients with drug-induced renal disease or unknown cause. Pregnant women with chronic kidney disease are excluded from the study. The research was conducted in150 patients in which common are men. The mean age of the research people was found to be 51.2 ±7. 02. .It was observed that calcium

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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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17

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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18

Radomski, Sidney B. "Update on medical therapy for male LUTS." Canadian Urological Association Journal 8, no. 7-8 (2014): 148. http://dx.doi.org/10.5489/cuaj.2310.

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The medical management of lower urinary tract symptoms (LUTS) is aimed at addressing voiding and storage symptoms in patients with benign prostate hyperplasia (BPH) symptoms with or without an overactive bladder (OAB). Current available options for BPH include the alpha-blockers, 5-alpha reductase inhibitors, and phosphodiesterase type 5 inhibitors. For OAB, options include antimuscarinics, with or without an alpha-blocker, the beta-3-adrenergic agonist mirabegron, and the synthetic diuretic desmopressin. With the availability of numerous options and combinations available for the treatment of

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19

Allon, M. "Hyperkalemia in end-stage renal disease: mechanisms and management." Journal of the American Society of Nephrology 6, no. 4 (1995): 1134–42. http://dx.doi.org/10.1681/asn.v641134.

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Clinical investigations in the past few years have enhanced the understanding of the mechanisms of hyperkalemia in patients with ESRD. The results of these studies have led to modifications in the acute treatment and prevention of hyperkalemia in this patient population. They have confirmed the efficacy of intravenous insulin, while raising doubts about the utility of intravenous bicarbonate, for the acute treatment of hyperkalemia. Moreover, the beta-adrenergic agonist albuterol has been shown to be a useful adjunct to insulin for acutely lowering plasma potassium. Finally, there has been enh

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20

Povetkin, S. V., V. I. Gikavyj, N. G. Bachinski, et al. "Comparative Pharmacoepidemiological Assessment of Antihypertensive Drugs Administration Structure in Pregnant Women in Routine Medical Practice in Kursk and Chisinau." Rational Pharmacotherapy in Cardiology 18, no. 5 (2022): 571–77. http://dx.doi.org/10.20996/1819-6446-2022-10-02.

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Aim. To study the structure of antihypertensive drugs prescription in pregnant women in routine practice in Kursk and Chisinau.Material and methods. The study design was observational descriptive cross-sectional. Authors conducted a survey of doctors in medical organizations in Kursk and Chisinau in 2017-2018.Results. Respondents from Kursk and Chisinau preferred methyldopa in prescriptions of central alpha-adrenergic receptor agonists. Doctors from Chisinau used clonidine in 14.3% of cases. The leading place in the group of calcium channel blockers belonged to short-acting nifedipine. Among b

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Jonkers, R., C. J. van Boxtel, R. P. Koopmans, and B. Oosterhuis. "A nonsteady-state agonist antagonist interaction model using plasma potassium concentrations to quantify the beta-2 selectivity of beta blockers." Journal of Pharmacology and Experimental Therapeutics 249, no. 1 (1989): 297–302. https://doi.org/10.1016/s0022-3565(25)23254-2.

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22

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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23

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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24

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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Kusumowardani, Alivia Retra. "60. Response to Revascularization in Resistant Hypertension Related to Renal Artery Stenosis: A Systematic Review of Case Reports." Journal of Hypertension 42, Suppl 2 (2024): e16. http://dx.doi.org/10.1097/01.hjh.0001027020.33700.fa.

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Background: Treatment for resistant hypertension related to renal artery stenosis is focused mainly through medical therapy. Revascularization is not routinely recommended due to its limited advantage over medical therapy. However, there have been reported cases of revascularization that has improved the patients’ outcome. Objective: This review of case reports is to identify the characteristics of patients who underwent revascularization and their response after follow up. Methods: A search through the Medline database for case reports of revascularization in renal artery stenosis published d

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Maltseva, A. S., A. E. Tsygankova, M. A. Gabitova, A. V. Rodionov, and V. V. Fomin. "Treatment of Resistant Hypertension in Real Clinical Settings." Rational Pharmacotherapy in Cardiology 17, no. 2 (2021): 200–205. http://dx.doi.org/10.20996/1819-6446-2021-04-03.

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Background. Current guidelines describe in detail the approaches to the management of patients with resistant hypertension, however, in real clinical settings the number of non-rational and ineffective combinations of antihypertensive drugs used remains high.Aim. To analyze the distribution of different combinations of antihypertensive drugs for the treatment of resistant hypertension and to estimate the proportion of non-rational combinations.Methods. The retrospective analysis includes 117 outpatients with resistant hypertension. Resistant hypertension was defined as blood pressure that rema

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27

Venglarik, C. J., R. J. Bridges, and R. A. Frizzell. "A simple assay for agonist-regulated Cl and K conductances in salt-secreting epithelial cells." American Journal of Physiology-Cell Physiology 259, no. 2 (1990): C358—C364. http://dx.doi.org/10.1152/ajpcell.1990.259.2.c358.

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We developed a convenient flux assay that permits simultaneous measurement of Cl and K conductance pathways in Cl-secreting epithelial cells. Monolayers of the colonic tumor cell line T84 were preloaded with 125I and 86Rb, and isotope effluxes were monitored by a sample-replace procedure. The adenosine 3',5'-cyclic monophosphate (cAMP)-mediated agonists forskolin and prostaglandin E2 increased I efflux with little effect on Rb efflux, whereas the Ca-mediated agonists ionomycin, A23187, and carbachol increased both I and Rb effluxes. Simultaneous determinations of I and Cl or Rb and K effluxes

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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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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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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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Priyanka, C. A., Jayanthi M. K., Pratibha Periera, and Ranjith Raj. "Analysis of prescription pattern of antihypertensive medication and adherence to Beers criteria in geriatric department of a tertiary care hospital in Mysuru." International Journal of Basic & Clinical Pharmacology 8, no. 12 (2019): 2669. http://dx.doi.org/10.18203/2319-2003.ijbcp20195275.

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Background: The objective of the present study was to evaluate the prescription pattern of anti-hypertensive drugs and adherence to Beers’ criteria in geriatric department of JSS Hospital, Mysuru.Methods: An observational, prospective, cross-sectional study was carried out in geriatric department. The basic demographic information and prescriptions of geriatric patients were studied. Descriptive analysis was used to present the results, prescriptions were analysed and checked for adherence to Beers’ criteria.Results: Out of 485 patients, 82.68% received monotherapy, 15.87% received 2-drug comb

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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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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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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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Godfraind, ThéOphile, Cécile Egleme та Iyad Al Osachie. "Role of endothelium in the contractile response of rat aorta to α-adrenoceptor agonists". Clinical Science 68, s10 (1985): 65s—71s. http://dx.doi.org/10.1042/cs068s065.

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1. The influence of endothelium on the response of rat isolated aorta to α-adrenergic agonists has been studied by comparing the response of intact and denuded preparations before and after treatment with calcium entry blockers flunarizine and nifedipine. 2. Endothelium removal enhanced the response of the preparations, especially to α2-agonists that had a weak effect in intact preparations. In the absence of endothelium, about 80% of the maximum response to clonidine was blocked by calcium entry blockers, whereas only 25% of the maximum response to noradrenaline was sensitive to them. In cont

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Sanaee, Forough, and Fakhreddin Jamali. "Action and Disposition of the β3-Agonist Nebivolol in the Presence of Inflammation; An Alternative to Conventional β1-Blockers." Current Pharmaceutical Design 20, no. 9 (2014): 1311–17. http://dx.doi.org/10.2174/13816128113199990550.

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Maccari, Sonia, Vanessa Vezzi, Federica Barbagallo та ін. "β-blockers Reverse Agonist-Induced β2-AR Downregulation Regardless of Their Signaling Profile". International Journal of Molecular Sciences 21, № 2 (2020): 512. http://dx.doi.org/10.3390/ijms21020512.

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Altered β-adrenergic receptor (β-AR) density has been reported in cells, animals, and humans receiving β-blocker treatment. In some cases, β-AR density is upregulated, but in others, it is unaffected or even reduced. Collectively, these results would imply that changes in β-AR density and β-blockade are not related. However, it has still not been clarified whether the effects of β-blockers on receptor density are related to their ability to activate different β-AR signaling pathways. To this aim, five clinically relevant β-blockers endowed with inverse, partial or biased agonism at the β2-AR w

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Silva-Néto, Raimundo Pereira, Carla Jevoux, and Abouch Krymchantowski. "Preventive and abortive treatment of migraine with traditional drugs. The state of the art." Headache Medicine 14, no. 3 (2023): 133–43. http://dx.doi.org/10.48208/headachemed.2023.27.

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IntroductionMigraine is a chronic neurological disease, with a prevalence of 15.2% in Brazil. It is 2.2 times more prevalent in women, predominantly in the 18-50 age group. Its pathophysiological mechanism is still not completely understood. Possibly headache attacks and symptoms are associated with cortical spreading depression, the trigeminovascular system, neurogenic inflammation, vasodilation and genetic vulnerability.ObjectiveThis is a narrative review of preventive and abortive treatment of migraine.CommentMigraine treatment is based on three pillars: patient education, treatment of the

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Prasad, Nitesh, and Kumari Suprema. "A Clinical Case of Beta-2 Agonist Induced Hypokalemia." Journal of Neonatal Surgery 14, no. 8S (2025): 76–81. https://doi.org/10.52783/jns.v14.2497.

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Background: Beta-2 adrenergic receptor agonists are extensively used in the management of bronchial asthma and chronic obstructive pulmonary disease (COPD). These agents can cause a variety of systemic adverse effects, most notably hypokalemia, by promoting the intracellular shift of potassium ions. Hypokalemia, defined as a serum potassium level below 3.5 mEq/L, may present with neuromuscular manifestations (e.g., weakness, cramps, paresthesia) and cardiovascular complications, such as arrhythmias and hypotension. Methods: We present the case of a 4-month-old male with a history of recurrent

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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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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 (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 i

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Kobayashi, S., M. C. Gong, A. V. Somlyo, and A. P. Somlyo. "Ca2+ channel blockers distinguish between G protein-coupled pharmacomechanical Ca2+ release and Ca2+ sensitization." American Journal of Physiology-Cell Physiology 260, no. 2 (1991): C364—C370. http://dx.doi.org/10.1152/ajpcell.1991.260.2.c364.

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The effects of Ca2+ channel blockers on two modes of G protein-mediated pharmacomechanical coupling, Ca2+ release and modulation of Ca2+ sensitivity of the contractile apparatus, were investigated. Smooth muscles were permeabilized with Staphylococcal alpha-toxin or with beta-escin to avoid effects due to block of sarcolemmal Ca2+ channels, while retaining receptor/G protein coupling. In permeabilized portal vein smooth muscle, verapamil and nifedipine inhibited Ca2+ release induced by an alpha 1-adrenergic agonist (phenylephrine) and by guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S), but n

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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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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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Il`ina, Inna V., Dana Z. Tlostanova, Svetlana A. Masjukova, Diana S. Urakova, Veronika V. Mordovtseva, and Igor A. Volchek. "Experience of using topical beta-blockers in combination therapy of rosacea." Consilium Medicum 27, no. 6 (2025): 323–27. https://doi.org/10.26442/20751753.2025.6.203312.

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Background. Neurovascular disorders and an imbalance of immune regulation are the leading links in the pathogenesis of rosacea. However, the basic therapeutic goal underlying the formation of clinical manifestations of rosacea has not been determined, so most treatment methods do not give the desired result. One of the “sniper” drugs is a highly selective α2-adrenergic receptor agonist with powerful vasoconstrictive activity brimonidine tartrate. Promising topical drugs are β-blockers. The mechanism of their action consists not only in vasoconstriction, but also in slowing the growth of vascul

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&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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&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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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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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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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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