Zusammenfassung
Um 1960 wurde beschrieben, daß das Gift der brasilianischen Grubenotter Bothrops Jararaca zur Bradykininpotenzierung führte (Ferreira 1965). Ferreira et al. (1970) extrahierten eine Fraktion aus dem Schlangengift und nannten sie nach ihrer Wirkung „bradykininpotenzierender Faktor“ (BPF). Die weitere pharmakologische Beschäftigung mit BPF zeigte, daß neben der Hemmung des Abbaus von Kininen durch die Kininase II zu inaktiven Fragmenten ebenfalls die Biosynthese von Angiotensin II (Ang II) aus Ang I durch das Ang I-Konversionsenzym blockiert wird. Er dös (1975) beschrieb dann, daß beide Vorgänge von ein und demselben Enzym katalysiert werden und stellte damit fest, daß die Kininase II mit dem Konversionsenzym identisch ist. Aus BPF wurden mehrere Peptide isoliert, von denen ein Nonapeptid, nämlich Teprotid, einen wirksamen Hemmstoff des Konversionsenzyms darstellte (Cheung u. Cushman 1973). Teprotid konnte aber nur parenteral appliziert werden und zeichnete sich außerdem durch eine kurze Halbwertszeit aus. So begann die Entwicklung synthetischer Konversionsenzymhemmstoffe, deren erster therapeutisch genutzter Vertreter Captopril war (Ferguson et al. 1977). Captopril wurde 1980 in Deutschland zur Behandlung der essentiellen Hypertonie in die Therapie eingeführt, 1984 folgte Enalapril. Im Jahre 1990/91 erschienen mit Perindopril, Lisinopril, Ramipril und Quinapril 4 weitere Konversionsenzymhemmer, die als 2. Generation bezeichnet wurden.
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Dominiak, P., Raasch, W. (1996). Pharmakologie der ACE-Hemmer. In: Dominiak, P., Bönner, G. (eds) ACE-Hemmer in Klinik und Praxis. Aktuelle Therapieprinzipien in Kardiologie und Angiologie. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-78376-0_3
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