Zusammenfassung
Die individuelle genetische Disposition — im Kontext mit Umweltfaktoren — beeinflußt die Manifestation und den Verlauf der essentiellen arteriellen Hypertonie. Grundlage für diese Erkenntnis waren in den 50er und 60er Jahren durchgeführte Familien-, Adoptions-, Geschwister- und Zwillingsstudien, die zeigen konnten, daß genetische und äußere Einflüsse zu etwa gleichen Teilen zur Genese der Erkrankung beitragen [Ward 1990]. Die anfänglich geäußerte Vermutung, daß in der Regel nur ein einzelner Gendefekt jeweils zur Entwicklung einer Hypertonie führt [Platt 1947], mußte jedoch verlassen werden. Pickering [1968] machte die Beobachtung, daß Patienten mit arterieller Hypertonie vielmehr das obere Ende einer Verteilungskurve repräsentieren (Abb. 4.1.1). Die quantitative Erfassung des Merkmals (Phänotyps) erlaubte rasch die Erkenntnis, daß die Regulation des arteriellen Blutdrucks multifaktoriell, d. h. durch die kombinierte Wirkung einer Vielzahl von Genen und äußeren Faktoren, kontrolliert wird [Mongeau et al. 1986].
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Schunkert, H. (1998). Kandidatengene der arteriellen Hypertonie und ihre klinische Bedeutung. In: Ganten, D., Ruckpaul, K. (eds) Herz-Kreislauf-Erkrankungen. Handbuch der Molekularen Medizin, vol 3. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-80360-4_10
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