gms | German Medical Science

27. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

Deutsche Liga zur Bekämpfung des hohen Blutdrucks – Deutsche Hypertonie Gesellschaft e. V.

26. bis 29.11.2003, Bonn

Blood Pressure is Regulated by Differential Binding of Transcription Factor E2F-2 to the Endothelin-Converting Enzyme-1b Promoter

Differentielle Bindung des Transkriptionsfaktors E2F-2 am Endothelin-Converting Enzym-1b Promotor reguliert Blutdruck

Meeting Abstract (Hypertonie 2003)

  • presenting/speaker H. Funke-Kaiser
  • F. Reichenberger
  • K. Köpke
  • S.M. Herrmann
  • J. Schönfelder
  • H.D. Orzechowski
  • W. Zidek
  • M. Paul
  • E. Brand

Hypertonie 2003. 27. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Bonn, 26.-29.11.2003. Düsseldorf, Köln: German Medical Science; 2004. Doc03hochV35

The electronic version of this article is the complete one and can be found online at:

Published: November 11, 2004

© 2004 Funke-Kaiser et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



The endothelin-converting enzyme (ECE)-1 gene is a candidate for human blood pressure (BP) regulation and we report the identification of the new gene variants T-839G, C-338A, L75F, A677V, and C+295T. Transient transfection of the reporter constructs containing the -338A allele showed an increase in promoter activity compared to the wild type promoter. EMSA revealed the specific binding of E2F-2 to both ECE-1b promoter sequences, with the -338A allele being associated with an increased affinity to E2F-2 compared to -338C. The clinical relevance of this finding was analyzed in 704 hypertensive patients. In untreated hypertensive women, both the -338A and -839G alleles, were significantly associated with ambulatory BP values. This study provides the first evidence of a link between the cell-cycle associated E2F family and BP regulation via a component of the endothelin system.