Propranolol inhibits IK(Ado) by competetive A1-receptor interaction
| العنوان: | Propranolol inhibits IK(Ado) by competetive A1-receptor interaction |
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| المؤلفون: | Bodo Brandts, Ingo Wickenbrock, D. Dirkmann, H.-J. Trappe, Rolf Borchard, M.W. Prull, M. van Bracht |
| المصدر: | Zeitschrift für Kardiologie. 93:533-539 |
| بيانات النشر: | Springer Science and Business Media LLC, 2004. |
| سنة النشر: | 2004 |
| مصطلحات موضوعية: | medicine.medical_specialty, Adenosine, Voltage clamp, Adrenergic beta-Antagonists, Propranolol, GTP-Binding Protein alpha Subunits, Gi-Go, Pharmacology, Binding, Competitive, Membrane Potentials, Adenosine A1 receptor, Adenosine Triphosphate, Internal medicine, Muscarinic acetylcholine receptor, Potassium Channel Blockers, medicine, Animals, Heart Atria, Cells, Cultured, Ion channel, Dose-Response Relationship, Drug, Receptor, Adenosine A1, business.industry, Receptors, Muscarinic, Acetylcholine, Rats, Endocrinology, Potassium Channels, Voltage-Gated, Cardiology and Cardiovascular Medicine, business, Anti-Arrhythmia Agents, Intracellular, medicine.drug |
| الوصف: | Betablocking agents are known to exert anti-arrhythmic effects in ischemic myocardium due to blockade of myocardial beta-1-receptors. Since adenosine (Ado) induced muscarinic potassium current (IK(Ado)) and ATP sensitive potassium current (IK(ATP)) are discussed to be activated during ischemia we studied the effect of propranolol on IK(Ado) and IK(ATP).The effect of propranolol on muscarinic potassium current and IK(ATP) was studied in isolated rat atrial myocytes by means of the whole-cell voltage clamp tech- nique. Propranolol (50 microM) completely inhibited IK(Ado). IC50 was 7 microM. Inhibition of acetylcholine induced current (IK(ACh)) and GTP-gamma-S induced muscarinic potassium current was less potent (IC50 29 microM and 31 microM respectively). Propranolol was active from the outside only. Intracellular application did not significantly affect muscarinic potassium current. (+)-propranolol, an isomer without beta-blocking properties, was as effective as (+/-)-propranolol. The inwardly rectifying potassium current IK(ATP) showed minor sensitivity to the compound (10% current reduction, propranolol 50 microM).Propranolol inhibits IK(Ado). Inhibition is not due to beta-receptor blockade. Predominantly an interaction with A1-receptors seems to be involved. The observations in part might explain the anti-arrhythmic properties of the drug in ischemic/fibrillating myocardium based on the prolongation of refractoriness. |
| تدمد: | 1435-1285 0300-5860 |
| DOI: | 10.1007/s00392-004-0094-0 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6fc3a8b6b269a29f4b8892a9297ec78d https://doi.org/10.1007/s00392-004-0094-0 |
| Rights: | CLOSED |
| رقم الانضمام: | edsair.doi.dedup.....6fc3a8b6b269a29f4b8892a9297ec78d |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 14351285 03005860 |
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| DOI: | 10.1007/s00392-004-0094-0 |