Zusammenfassung
Die Wirkung einer medikamentösen ACE-Hemmung besteht in einer verminderten Bildung von Angiotensin II aus Angiotensin I. An dieser Bildung sind allerdings auch andere Enzymsysteme beteiligt. Ebenfalls gehemmt wird der Abbau von Bradykinin. Angiotensin II wirkt stark vasokonstringierend im arteriellen, aber auch im venösen System. Es f#x00FC;hrt zu einer vermehrten Freisetzung von Aldosteron und Catecholaminen. Nachgewiesen wurden außerdem trophische Effekte in Zellkulturen, die Bedeutung für die vaskulären und kardialen Veränderungen bei Hochdruck- und Nierenkrankheiten haben. Untersuchungen mit den neueren Angiotensinrezeptorantagonisten zeigten, daß die Rezeptoren für Angiotensin II in mindestens zwei Gruppen, AT1 und AT2-Rezeptoren, mit teilweise gegensätzlichen Effekten gegliedert werden müssen. Die antihypertensive Wirkung erfolgt über AT1-Rezeptorblockade, während der AT2-Rezeptor weiterhin der Wirkung des Angiotensins ausgesetzt ist. Dies und der nicht gehemmte Abbau von Bradykinin gestatten nicht die ungeprüfte Annahme einer gleichen klinischen Wirksamkeit von ACE-Hemmern und Angiotensinrezeptorantagonisten oder gar die voreilige Behauptung, Angiotensinrezeptorantagonisten seien lediglich besser verträgliche ACEHemmer.
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Anlauf, M. (2004). ACE-Hemmer und Angiotensinrezeptorantagonisten. In: Schwabe, U., Paffrath, D. (eds) Arzneiverordnungs-Report 2003. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-18512-0_3
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