Zusammenfassung
Heute ist allgemein anerkannt, daß ein erhöhter peripherer Gesamtwiderstand das hämodynamische Kennzeichen nahezu aller Formen der klinischen Hypertonic in alien Stadien der Erkrankung ist. Es erscheint daher logisch, diese Erkrankung mit Antihypertensiva zu behandeln, die einen oder mehrere vasokonstriktorische Mechanismen beeinflussen, um die zugrundeliegende hämodynamische Anomalie zur Umkehr zu bringen. Tatsächlich scheinen die meisten antihypertensiven Substanzklassen eine solche Wirkung auf die Widerstandsgefäße aufzuweisen. In einem neueren und umfassenden Überblick zum Thema stellte Lund- Johansen, einer der Pioniere auf dem Gebiet der hämodynamischen Forschung bei Hypertonic, 154 Arbeiten zur Hämodynamik bei Hypertonic und zu deren medikamentöser Behandlung zusammen [1]. Aus seiner Arbeit und der anderer Autoren geht hervor, daß tatsächlich die meisten Gruppen von Antihypertensiva vasokonstriktorische Mechanismen beeinflussen, da die Mehrzahl den Gefäßwiderstand bis zu einem gewissen Grad senkt (Abb. 1).
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Man in ’t Veld, A.J., v.d. Meiracker, A.H., Schalekamp, M.A. (1997). Führen β-Blocker tatsächlich zu einer Zunahme des peripheren Gefäßwiderstands?. In: Dominiak, P., Hjalmarson, A., Kendall, M.J., Kübler, W., Olsson, G. (eds) Betablocker — im Mittelpunkt der Forschung. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60716-5_10
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