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Pharmakologie und klinische Pharmakologie der AT1-Rezeptorantagonisten

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Zusammenfassung

Seit 1980 standen mit den ACE-Hemmern (damals Captopril) erstmals Substanzen für die antihypertensive Therapie in Deutschland zur Verfügung, die ihre Angriffspunkte am Renin-Angiotensin-Aldosteron-System (RAAS) hatten und nicht, wie die bis zu diesem Zeitpunkt verfügbaren Antihypertensiva, die auf das sympathische System (zentral oder peripher), an der Niere oder auf die glatte Muskulatur wirkten. Auch ß-Adrenozeptoranta- gonisten beeinflussen das RAAS, indem sie die ß1-Adrenozeptoren am juxtaglomerulären Apparat der Niere blockieren und so zu einer verminderten Bildung und Freisetzung des Schlüsselenzyms für die Angiotensin (Ang)-II-Biosynthese, des Renins, beitragen, aber dies ist nicht ihre Hauptwirkung.

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Dominiak, P., Dendorfer, A. (1999). Pharmakologie und klinische Pharmakologie der AT1-Rezeptorantagonisten. In: Dominiak, P., Unger, T. (eds) Angiotensin II AT1-Rezeptorantagonisten. Steinkopff, Heidelberg. https://doi.org/10.1007/978-3-642-93705-7_2

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