PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 10629868-5 1999 Propranolol and bopindolol have high affinity to beta 1 and beta 2 subtypes, but low affinity to beta 3 subtype. Propranolol 0-11 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 49-66 9846642-14 1998 Treatment of hamsters with propranolol resulted in increased density of beta1-adrenoceptors in both strains, but had no effect on their functional efficacy. Propranolol 27-38 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 72-77 1541316-3 1992 Equivalent doses of the pure antagonists atenolol (beta 1) and propranolol (beta 1, beta 2) produced similar reductions in heart rate, systolic blood pressure, and cardiac index, and increases in stroke volume and total peripheral resistance, particularly during exercise. Propranolol 63-74 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 76-90 7701450-8 1995 Whilst propranolol blunted exercise heart rate in keeping with beta 1 blockade, salbutamol had no effect. Propranolol 7-18 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 63-69 8658370-7 1996 Propranolol blunted the heart rate delta response to exercise, consistent with beta 1 blockade, whilst salmeterol and formoterol had no effect. Propranolol 0-11 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 79-85 7567595-9 1995 After administration of beta 1-, beta 2-blocker, propranolol (30 mg/day), cAMP at 3 minutes of tilt decreased significantly compared to the baseline tilt (16.9 +/- 1.4 pmol/mL vs 25.3 +/- 2.0 pmol/mL; P < 0.05) and propranolol prevented the syncope in all six patients. Propranolol 218-229 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 24-31 7912102-0 1993 Extent of beta 1- and beta 2-receptor occupancy in plasma assesses the antagonist activity of metoprolol, pindolol, and propranolol in the elderly. Propranolol 120-131 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 10-16 7912102-1 1993 We estimated antagonist activity of metoprolol, pindolol, and propranolol in elderly cardiovascular patients by determining the extent to which the drugs occupied rabbit lung beta 1- and rat reticulocyte beta 2-adrenoceptors in plasma samples during drug treatment. Propranolol 62-73 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 175-181 7912102-5 1993 The results and conclusions were the following: (a) The extent to which metoprolol, pindolol, and propranolol occupied rabbit lung beta 1- and rat reticulocyte beta 2-adrenoceptors in plasma samples estimated accurately the intensity of beta-receptor antagonism in the patients who did not tolerate physiological and pharmacological tests measuring the degree of beta 1- and beta 2-adrenoceptor blockade. Propranolol 98-109 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 131-137 7912102-6 1993 (b) The mean beta 1- and beta 2-receptor occupancy of pindolol and propranolol varied between 76% and 99% during the treatments. Propranolol 67-78 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 13-19 8104518-2 1993 beta 1-Adrenolytic (atria) structure-activity correlations indicated that replacement of the 1-naphthyl moiety of propranolol by a 4-quinolyl- (10), 2-quinolyl- (24), or 2-pyrimidyl- (26) heterocyclic moiety resulted in a 10-16 fold reduction in activity. Propranolol 114-125 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 0-6 1717272-2 1991 This effect is stereoselectively inhibited by (-)-propranolol and is inhibited also by the beta 1-selective adrenergic antagonists, bisoprolol and metoprolol. Propranolol 46-61 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 91-97 1659260-3 1991 Aerosol administration of the beta antagonists, propranolol (beta 1 and beta 2), atenolol (beta 1), and butoxamine (beta 2) decreased dynamic compliance (Cdyn) and increased pulmonary resistance (RL) in the principal ponies during airway obstruction, but were without effect when the ponies were in clinical remission. Propranolol 48-59 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 61-78 1659260-3 1991 Aerosol administration of the beta antagonists, propranolol (beta 1 and beta 2), atenolol (beta 1), and butoxamine (beta 2) decreased dynamic compliance (Cdyn) and increased pulmonary resistance (RL) in the principal ponies during airway obstruction, but were without effect when the ponies were in clinical remission. Propranolol 48-59 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 61-67 1671724-3 1991 For example, propranolol is a nonselective beta-blocker with antagonist effects on both beta 1 and beta 2 receptors, atenolol is a selective beta 1-antagonist, and celiprolol is a selective beta 1-antagonist, partial beta 2-agonist. Propranolol 13-24 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 88-94 1845926-6 1991 Preinduction K+ changes were determined in patients given a single preoperative dose of propranolol (beta 1/beta 2-antagonist), atenolol (beta 1-antagonist), or no beta-blocker (control). Propranolol 88-99 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 101-107 2901818-7 1988 INTERVENTION: The beta-1-nonselective blocker was propranolol, 80 mg twice daily. Propranolol 50-61 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 18-24 2866062-3 1985 In a cross-over trial of placebo, atenolol (beta 1-blocker), propranolol (beta 1- and beta 2-blocker) and pindolol (beta 1- and beta 2-blocker with intrinsic sympathomimetic activity) in 11 normal men t1/2 was 11.8 +/- 0.9, 12.6 +/- 1.1, 14.3 +/- 1.7 and 12.4 +/- 1.1 min respectively. Propranolol 61-72 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 74-80 3520212-1 1986 We have previously shown that the increase in energy expenditure following glucose/insulin infusion is, in large part, mediated by the sympathetic nervous system and that this sympathetic component can be blocked by the nonselective beta-1, beta-2 antagonist propranolol. Propranolol 259-270 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 233-239 2839668-5 1988 After propranolol administration, in vitro beta-1 and beta-2 adrenoceptor occupancy declined from initially 97% to less than 10% within 48 hr. Propranolol 6-17 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 43-49 3017797-3 1986 The adrenergic receptor mediating the adrenaline effect was characterized by concomitant infusion of propranolol (beta 1 + beta 2-antagonist) or metoprolol (beta 1-antagonist). Propranolol 101-112 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 114-120 2439798-9 1986 Assessing the data for a beta 1/beta 2-splitting as 1 for propranolol, the relative beta 1-selectivity (mean +/- SEM) was 12.2 +/- 1.1 for bisoprolol, 9.0 +/- 0.9 for metoprolol, 6.2 +/- 0.6 for acebutolol, and 0.6 +/- 0.06 for penbutolol. Propranolol 58-69 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 25-31 2439798-9 1986 Assessing the data for a beta 1/beta 2-splitting as 1 for propranolol, the relative beta 1-selectivity (mean +/- SEM) was 12.2 +/- 1.1 for bisoprolol, 9.0 +/- 0.9 for metoprolol, 6.2 +/- 0.6 for acebutolol, and 0.6 +/- 0.06 for penbutolol. Propranolol 58-69 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 84-90 6281414-9 1982 Increases in the densities of beta-1 and/or beta-2 adrenergic receptors in solid tissues may be related to some of the untoward effects observed in humans after abrupt discontinuation of propranolol administration. Propranolol 187-198 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 30-41 6199591-8 1984 beta-Blockade with propranolol (nonselective), 80 mg four times a day, or atenolol (beta 1-selective), 100 mg once a day, antagonized the hypokalemic effect of isoproterenol as well as the rise in norepinephrine, but when isoproterenol was infused in doses high enough to overcome the blockade of the heart rate response, the effects on norepinephrine and potassium were abolished by propranolol and not by atenolol. Propranolol 384-395 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 84-90 6130932-1 1983 The influence of acute beta 1-receptor blockade using 50 mg metoprolol or beta 1/beta 2-blockade using 40 mg propranolol resulted in an equipotent reduction of cardiac frequency and systolic blood pressure without influencing diastolic pressure in ten healthy probands. Propranolol 109-120 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 23-29 6130932-1 1983 The influence of acute beta 1-receptor blockade using 50 mg metoprolol or beta 1/beta 2-blockade using 40 mg propranolol resulted in an equipotent reduction of cardiac frequency and systolic blood pressure without influencing diastolic pressure in ten healthy probands. Propranolol 109-120 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 74-87 6138298-5 1983 SCC was not influenced by the beta 1-antagonist atenolol but was modified, although differently in rabbit and man, by the beta 1- and beta 2-antagonist propranolol. Propranolol 152-163 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 122-140 6188919-6 1983 It has been demonstrated that beta-blockers with intrinsic sympathomimetic activity (ISA), such as pindolol, and beta 1-selective blockers have a less marked effect on pulmonary function than nonselective beta-blockers without ISA, such as propranolol. Propranolol 240-251 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 113-119 7259364-7 1981 Under the experimental conditions of this trial, propranolol inhibited beta 1 and beta 2 receptors at the same time, whereas acebutolol inhibited only beta 1 receptors. Propranolol 49-60 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 71-77 6113715-2 1981 In contrast to Talinolol under the treatment ith the unspecific beta-blocker Propranolol a clear blocking of the beta 2-mediated glycogenolysis which can be evoked with the help of Orciprenalin and of the lipolysis evocable via beta 1-receptors was observed. Propranolol 77-88 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 228-234 190674-2 1977 In this study it was shown that tremor caused by terbutaline could be blocked by propranolol, a drug with both beta1- and beta2-blocking properties, but not by metoprolol, a beta1-selective antagonist. Propranolol 81-92 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 111-127 13495-2 1977 When given in equipotent beta1 blocking doses, the nonselective blocker propranolol and the beta1 selective blocker metoprolol differ markedly as regards inhibition of adrenaline induced beta2 mediated vasodilatation. Propranolol 72-83 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 25-30 28240622-2 2017 Propranolol, a nonselective beta1, beta2-adrenergic receptor antagonist, reduces resting heart rate and cardiac work caused by elevated circulating catecholamines. Propranolol 0-11 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 28-33 31296894-4 2019 Propranolol, a non-specific beta1-and beta2-adrenergic receptor antagonist, was recently designated as the first therapeutic (orphan) drug for VHL disease. Propranolol 0-11 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 28-33 29210030-6 2018 Propranolol and nadolol block the beta-1 in the heart and the peripheral beta-2 adrenergic receptors. Propranolol 0-11 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 34-40 11306460-4 2001 The beta1/2-blocker propranolol but not the beta1-blocker atenolol inhibited this increase. Propranolol 20-31 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 4-11 18403423-5 2008 Administration of a non-selective beta-adrenergic (beta(1) + beta(2)) receptor antagonist (propranolol) reduced heart rate (69 +/- 8 to 58 +/- 6 beats min(-1)) and exercise capacity (239 +/- 42 to 209 +/- 31 W; P < 0.05) with arterial lactate reaching 9.4 +/- 3.6 mm. Propranolol 91-102 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 34-58 28556385-1 2017 BACKGROUND/OBJECTIVES: The nonselective beta-blocker propranolol is the current criterion standard for treatment of infantile hemangiomas (IHs) and the first therapy that the U.S. Food and Drug Administration has approved for the condition, but concern about adverse effects, such as bronchospasm, hypoglycemia, and sleep disturbances, has sparked interest in the use of alternative agents such as the selective beta1 antagonist atenolol. Propranolol 53-64 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 412-417 20424515-6 2010 beta2-adrenergic antagonist ICI118,551 and beta1/2-adrenergic antagonist propranolol significantly suppressed cell invasion and proliferation in comparison to beta1-adrenergic antagonist metoprolol and control in a Matrigel invasion assay and subrenal capsular assay. Propranolol 73-84 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 43-50 20424515-6 2010 beta2-adrenergic antagonist ICI118,551 and beta1/2-adrenergic antagonist propranolol significantly suppressed cell invasion and proliferation in comparison to beta1-adrenergic antagonist metoprolol and control in a Matrigel invasion assay and subrenal capsular assay. Propranolol 73-84 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 43-48 17414346-1 2007 BACKGROUND: Propranolol, a nonselective beta1-2 antagonist, attenuates hypermetabolism and catabolism in severely burned patients. Propranolol 12-23 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 40-47 15710352-4 2005 The involvement of beta-adrenergic receptors was confirmed using the general beta(1)/beta(2) receptor antagonist propranolol, which was able to abrogate the protection conferred by isoproterenol and clenbuterol in astrocytes treated with LPS. Propranolol 113-124 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 77-84 11141226-13 2001 Whenever beta-blockers are chosen for treatment of hyperthyroidism, propranolol (beta 1 + beta 2) has an advantage because it reduces the metabolic rate, whereas selective beta 1-blockade seemed to provide only symptomatic relief, related to the normalization of heart rate. Propranolol 68-79 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 81-96 11141226-13 2001 Whenever beta-blockers are chosen for treatment of hyperthyroidism, propranolol (beta 1 + beta 2) has an advantage because it reduces the metabolic rate, whereas selective beta 1-blockade seemed to provide only symptomatic relief, related to the normalization of heart rate. Propranolol 68-79 potassium calcium-activated channel subfamily M regulatory beta subunit 1 Homo sapiens 81-87