Zusammenfassung
Es ist allgemein anerkannt, daß das Renin-Angiotensin-System nicht nur ein endokrines, sondern auch ein parakrines oder autokrines System ist, da alle seine Komponenten auf Gewebeebene generiert oder aktiviert werden. Technische Fortschritte in der Biochemie und Molekularbiologie führten zur Identifizierung der einzelnen Komponenten des Renin-Angiotensin- Systems in vielen Geweben und zur Aufdeckung ihrer Struktur-Wirkungsbeziehung. Neuere Befunde belegen außerdem nachdrücklich, daß die Ang-II-bildende Gewebesysteme eine bedeutsamere physiologische Rolle als ursprünglich gedacht spielen [34, 36]. Sie tragen zur kardiovaskulären Homöostase bei und sind wahrscheinlich beim „remodeling“ kardiovaskulärer Gewebe beteiligt. Zudem haben Beobachtungen, die im wesentlichen auf dem Einsatz von Medikamenten basieren, welche mit dem Renin-Angiotensin-System interferieren, das Interesse auf der pathophysiologischen Bedeutung lokaler Renin-Angiotensin-Systeme gelenkt. Die erfolgreiche Einführung der ACE-Inhibitoren in die Therapie von Patienten mit kardiovaskulären Erkrankungen weist auf eine bedeutsame Rolle sowohl des systemischen als auch lokaler Renin-Angiotensin-Systeme hin.
Dieses Projekt wird zum Teil unterstützt durch Forschungsstipendien der EG-Kommission (PL930076) und der Alexander von Humboldt-Gesellschaft (IV1-7121)
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Urata, H. et al. (1996). Mechanismus der Gewebe-Angiotensin-II-Bildung im Herzen und neue Befunde zum kardialen Angiotensin-II-System. In: Philipp, T., Schäfers, R.F. (eds) Angiotensin II — Antagonismus. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-79645-6_2
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