Zusammenfassung
Betarezeptorstimulation führt zu einer Aktivierung des membranständigen Enzyms Adenylatzyklase, welches durch Guaninnukleotid-stimulierende bzw. –inhibierende Faktoren moduliert wird und schließlich die Umwandlung von Adenosinphosphat (ATP) in zyklisches Adenosinmonophosphat (cAMP) induziert (6). Zyklisches AMP bewirkt 1. während der Systole eine Zunahme des freien intrazellulären Kalziums durch Phosphorylierung der Kalziumkanäle (positiv inotrope Wirkung), 2. Während der Diastole eine gesteigerte Wiederaufnahme von freiem Kalzium aus dem Zytosol des Myozyten in das sarkoplasmatische Retikulum (positiv lusitrope Wirkung) und 3. eine erhöhte Empfindlichkeit der kontraktilen Proteine für Kalzium (4, 17, 34). Alle Betablocker, die derzeit mit den verschiedensten klinischen Indikationsstellungen zur Behandlung von Bluthochdruck, koronarer Herzkrankheit, Rhythmusstörungen, Migräne oder Glaukom eingesetzt werden, entfalten ihre Wirkung über einen kompetitiven Antagonismus von ß-Adrenozeptoren. Die einzelnen Betablocker unterscheiden sich dabei in ihren pharmakologischen Eigenschaften, etwa der Selektivität für ß1bzw. ß2-Rezeptoren, dem möglichen Vorliegen einer intrinsischen sympathomimetischen Komponente (ISA), ihrer Fettlöslichkeit und/oder lokalanästhetischen Wirkung.
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© 1991 Dr. Dietrich Steinkopff Verlag, GmbH Co. KG, Darmstadt
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Stefenelli, T., Weber, H. (1991). Betablocker: Wer soll behandelt werden?. In: Schmidt, G. (eds) Medikamentöse Behandlung des Postinfarktpatienten nach CAST. Steinkopff. https://doi.org/10.1007/978-3-642-85414-9_10
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