PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 8789768-2 1996 Recently the beta-2 stimulatory drug salbutamol has been shown to be an effective agent to treat hyperkalaemia by inducing a shift of potassium into the intracellular compartment. Potassium 134-143 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 13-19 10339950-5 1999 In addition, attention should be paid to factors causing an additional reduction in the serum potassium concentration, such as alkalosis, elevated beta 2-adrenergic activity, increased availability of insulin and hypothermia. Potassium 94-103 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 147-153 10099101-4 1998 Medications generally produce hyperkalemia either by causing redistribution of potassium (beta2 -adrenergic blockers, succinylcholine, digitalis overdose, hypertonic mannitol) or by impairing renal potassium excretion. Potassium 79-88 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 90-95 8777958-8 1996 Serum potassium was significantly lower both before (4.0 +/- 0.2 mmol.L-1) and after (3.9 +/- 0.2 mmol.L-1) the withdrawal of oral beta 2-agonists compared with the control group (4.2 +/- 0.2 mmol.L-1). Potassium 6-15 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 131-137 7790611-2 1995 We refer to a patient with a brain stem compression after head injury, who developed a profound hypokalemia (K+ = 1.2 mmol/l) with life-threatening arrhythmias, probably due to a catecholamine induced intracellular potassium shift (beta-2-stimulation). Potassium 215-224 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 232-238 11092145-2 2000 Various conventional therapies including intravenous sodium bicarbonate, insulin with glucose and several beta-2 agonists are commonly employed as transient measures to enhance shift of potassium from the extracellular to the intracellular compartment. Potassium 186-195 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 106-112 8797398-10 1996 Both beta 2-agonists caused a decrease in serum potassium level that was significantly greater in the fenoterol (0.23 +/- 0.04 mmol/L) than in the salbutamol (0.06 +/- 0.03 mmol/L) group (p = 0.0002). Potassium 48-57 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 5-11 8832156-4 1996 However, recently also the beta 2 stimulatory drug salbutamol has been shown to be an effective agent to treat hyperkalemia by inducing a shift of potassium into the intracellular compartment. Potassium 147-156 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 27-33 7921529-6 1994 Both beta 2-agonists significantly decreased plasma potassium. Potassium 52-61 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 5-11 8315226-11 1993 The greater rate of increase in potassium in healthy and athletic subjects supports the hypothesis of an age-related impairment of the beta 2-adrenergic process that mediates potassium flux into skeletal muscle. Potassium 32-41 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 135-141 8315226-11 1993 The greater rate of increase in potassium in healthy and athletic subjects supports the hypothesis of an age-related impairment of the beta 2-adrenergic process that mediates potassium flux into skeletal muscle. Potassium 175-184 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 135-141 1429916-5 1992 This suggests that in asthmatic subjects on beta 2-agonist treatment, plasma potassium could be used as a surrogate marker for beta 2 activity at bronchi. Potassium 77-86 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 44-50 1429916-5 1992 This suggests that in asthmatic subjects on beta 2-agonist treatment, plasma potassium could be used as a surrogate marker for beta 2 activity at bronchi. Potassium 77-86 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 127-133 1429916-6 1992 It also implies that the most effective beta 2-agonist bronchodilators will produce the greatest fall in plasma potassium. Potassium 112-121 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 40-46 2370646-2 1990 We have previously demonstrated, by giving an infusion of terbutaline to human volunteers, that beta 2-stimulation causes a rise in plasma glucose and a fall in plasma potassium. Potassium 168-177 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 96-102 1768353-1 1991 For several years now, it has been known that the administering of adrenergic beta antagonists, especially of the beta-2 type, induce hypokalemia as a result of the entering of potassium into the skeletal muscle cells. Potassium 177-186 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 114-120 2747008-1 1989 Plasma potassium lowering effect of a selective beta-2 adrenergic stimulant, terbutaline sulfate (TRB) was investigated in fourteen patients with chronic renal failure (CRF) receiving maintenance hemodialysis. Potassium 7-16 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 48-54 2573312-1 1989 Administration of the beta 2 adrenergic agonists fenoterol, salbutamol and terbutaline to volunteers significantly reduced plasma potassium concentration in a double-blind crossover study. Potassium 130-139 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 22-28 2602234-0 1989 Cardiac arrhythmias during acute exacerbations of chronic airflow limitation: effect of fall in plasma potassium concentration induced by nebulised beta 2-agonist therapy. Potassium 103-112 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 148-154 2602234-1 1989 The effect on cardiac rhythm of the fall in plasma potassium concentration induced by nebulised beta2-agonist therapy was studied in 20 patients admitted to hospital with an acute exacerbation of their reversible chronic airflow limitation. Potassium 51-60 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 96-101 1970125-0 1990 [Decrease in serum potassium level caused by beta 2-sympathicomimetics]. Potassium 19-28 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 45-51 2308263-8 1990 Thus, the higher rise in potassium concentration during exercise with propranolol could only be explained by adrenergic blockade at the beta-2 receptor site. Potassium 25-34 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 136-142 2308263-9 1990 These results support the concept that adrenergic control of extrarenal potassium homeostasis in dialysis patients is mediated at the beta-2 receptor. Potassium 72-81 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 134-140 2308263-10 1990 Since a deterioration in potassium homeostasis during exercise is observed with beta-2, but not beta-1 blockade, selective beta-1 adrenergic blocking agents may be safer in dialysis patients. Potassium 25-34 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 80-86 2747008-6 1989 Thus, a beta-2 selective adrenergic stimulant, terbutaline sulfate may be useful for acute treatment of hyperkalemia in CRF patients by way of the stimulation of potassium uptake in the cells. Potassium 162-171 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 8-14 2838285-1 1988 Since the serum potassium level is under beta 2-adrenergic influence, we studied serum potassium values on admission in psychiatric patients. Potassium 16-25 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 41-47 2898368-0 1988 Decrease of plasma potassium due to inhalation of beta-2-agonists: absence of an additional effect of intravenous theophylline. Potassium 19-28 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 50-56 2898368-1 1988 The effect on the plasma potassium concentration of inhalation of the beta-2-agonists fenoterol, salbutamol (albuterol), and terbutaline from metered-dose inhalers was studied in normal volunteers. Potassium 25-34 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 70-76 3827459-8 1987 beta 2-adrenergic stimulation of intracellular potassium uptake by albuterol is a safe and effective alternative for the treatment of hyperkalemia in renal failure. Potassium 47-56 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 0-6 6143631-7 1984 This suggests that adrenaline acts via beta 2 adrenoceptors in man to cause potassium influx and systemic hypokalaemia. Potassium 76-85 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 39-45 2863970-1 1985 Experimental evidence is presented that activation of beta 2 adrenoreceptors causes a dose-dependent decrease in plasma potassium, probably by shifting potassium into the cell. Potassium 120-129 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 54-60 2863970-1 1985 Experimental evidence is presented that activation of beta 2 adrenoreceptors causes a dose-dependent decrease in plasma potassium, probably by shifting potassium into the cell. Potassium 152-161 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 54-60 2860336-7 1985 Inhalation of beta 2-agonists may be dangerous, especially in patients under stress--eg, during an acute asthmatic attack, when the plasma potassium concentration would already be subnormal as the result of raised circulating adrenaline levels. Potassium 139-148 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 14-20 4008616-3 1985 This led us to study the effect of the intravenous administration of salbutamol, a specific beta-2-adrenergic agonist, on serum potassium in 9 healthy subjects and in 23 patients with allergic asthma and/or rhinitis. Potassium 128-137 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 92-98 6318223-0 1983 Increase in serum potassium caused by beta-2 adrenergic blockade in terminal renal failure: absence of mediation by insulin or aldosterone. Potassium 18-27 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 38-44 16445274-7 2006 Serum potassium levels can be lowered acutely by using intravenous insulin and glucose, nebulized beta2 agonists, or both. Potassium 6-15 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 98-103 23988599-9 2013 Beta-2-adrenergic agonists and several other medications can affect serum potassium levels; although the potential risks posed by the use of such drugs in patients with a history of HPP are unclear, cautious use in the context of known HPP is advised. Potassium 74-83 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 0-6 15189956-9 2004 A single dose of beta(2)-agonist increased the heart rate by 9.12 beats/min (95% confidence interval [CI], 5.32 to 12.92) and reduced the potassium concentration by 0.36 mmol/L (95% CI, 0.18 to 0.54), compared to placebo. Potassium 138-147 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 17-23 15350154-16 2004 The long-acting beta2-agonists cause predictable adverse effects including headache, tremor, palpitations, muscle cramps and a fall in serum potassium concentration. Potassium 141-150 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 16-21