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Kallikrein-Kinin- und Prostaglandin-Systeme bei Hypertonie

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Arterielle Hypertonie

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Zusammenfassung

Der Beginn mancher Formen von Hypertonie sowie die Entwicklung der akzelerierten Phase der essentiellen Hypertonie spiegelt das Wirken eines oder mehrer hormonaler Pressorfaktoren wider, wie z. B. gesteigerte Aktivität des Renin-Angiotensin-Systems oder Mineralokortikoidüberschuß. Von nicht geringerer Bedeutung für die Blutdruckregulation ist das Versagen von Gegenkräften, die normalerweise eine Senkung des Blutdrucks bewirken. Das Kallikrein-Kinin-System besitzt die erforderlichen Eigenschaften, diese Funktion wahrzunehmen, insbesondere wenn man es unter dem Aspekt seiner Wechselwirkung mit Prostaglandinen betrachtet [84] (Abb. 1). Ein Ausbleiben der normalen Ausgleichsfunktion kann eine anhaltende Hypertonie verursachen ohne Aktivitätszunahme irgendeines Pressorfaktors. So kann, wenn man von der tonischen Aktivität entgegenwirkender Blutdruckregulationssysteme ausgeht, eine Dysfunktion im Vasodepressorsystem zu Hypertonie führen, ohne daß eine Zunahme der Grundaktivität des blutdruckerhöhenden Systems erfolgt. Innerhalb der Niere, und wahrscheinlich auch in den extrarenalen Blutgefäßen, stehen Prostaglandine in Wechselwirkung mit den hauptsächlichen Blutdruckregulationssystemen, dem Kallikrein-Kinin-System und dem adrenerg inner-vierten Renin-Angiotensin-System, unter Verstärkung des ersteren und Pufferung des letzteren [143]. Damit tragen Prostaglandine zur blutdrucksenkenden Wirkung der Kinine bei und machen die blutdruckerhöhende Wirkung von Angiotensinen zunichte. Eine verminderte Reaktionsfähigkeit des renalen Kallikreinsystems zeigte sich bei einigen Formen von Hypertonie beim Menschen und im Experiment [63, 79].

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  1. J. M. Sullivan
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  2. J. C. McGiff
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  1. Zentrum Innere Medizin, Universität Ulm, Steinhövelstr. 9, D-7900, Ulm, Deutschland

    Julian Rosenthal

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Sullivan, J.M., McGiff, J.C. (1984). Kallikrein-Kinin- und Prostaglandin-Systeme bei Hypertonie. In: Rosenthal, J. (eds) Arterielle Hypertonie. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-00760-0_15

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  • DOI: https://doi.org/10.1007/978-3-662-00760-0_15

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