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Lokale Expression und pathophysiologische Rolle von Renin-Angiotensin im Gefäßsystem und im Herzen

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Zusammenfassung

Während das zirkulierende Renin-Angiotensin-System (RAS) bei der kurzfristigen Aufrechterhaltung der kardiovaskulären Homöostase eine wichtige Rolle spielt, weisen neueste Studien darauf hin, daß das endogene RAS in Zielgeweben eine Rolle bei der langfristigen kardiovaskulären Regulation spielt. Dieser Artikel konzentriert sich auf die verschiedenen Wirkungen des Angiotensin Converting Enzyme (ACE) im Gewebe und von Angiotensin II (Ang II), seinem aktiven Peptidprodukt. Von Angiotensin II wurde nachgewiesen, daß es in glatten Gefäßmuskelzellen ein potenter Wachstumsfaktor ist. Je nach den lokalen Gegebenheiten kann die vaskuläre Reaktion eine Hypertrophie oder eine Hyperplasie sein. Die molekularen Mechanismen, die bei den Interaktionen von Angiotensin II mit Zellprodukten aus Endothel- oder glatten Muskelzellen beteiligt sind, können bei der Modulation der Gefäßstruktur bei der Hypertonie und bei einer Gefäßschädigung eine wichtige Rolle spielen. Auch gibt es Hinweise dafür, daß Angiotensin II bei der Entwicklung einer linksventrikulären Hypertrophie beim Hochdruck eine Rolle spielt. Darüber hinaus kann das kardiale RAS zur Pathophysiologie der Herzinsuffizienz beitragen. Experimentelle und klinische Studien mit ACE-Hemmern deuten darauf hin, daß die ACE-Aktivität im Gewebe bei der Entwicklung der Atherosklerose, bei der kardialen Hypertrophie und beim kardialen Umbau von Bedeutung ist.

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Dzau, V.J. (1993). Lokale Expression und pathophysiologische Rolle von Renin-Angiotensin im Gefäßsystem und im Herzen. In: Grobecker, H., Heusch, G., Strauer, B.E. (eds) Angiotensin und Herz. Steinkopff, Heidelberg. https://doi.org/10.1007/978-3-662-11145-1_1

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