gms | German Medical Science

29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

Deutsche Hochdruckliga e. V. DHL ® - Deutsche Hypertonie Gesellschaft Deutsches Kompetenzzentrum Bluthochdruck

23. bis 25.11.2005, Berlin

Renal ACE2 mRNA-expression and activity in the spontaneously hypertensive stroke-prone rat model of hypertension

Renale ACE2-Expression und Aktivität im hypertensiven SHRSP Rattenmodell

Meeting Abstract

  • I. Nassar - Charité Campus Benjamin Franklin, Berlin (Berlin, D)
  • R. Kreutz - Charité Campus Benjamin Franklin, Berlin (Berlin, D)
  • J. Bolbrinker - Charité Campus Benjamin Franklin, Berlin (Berlin, D)
  • M. Wehland - Charité Campus Benjamin Franklin, Berlin (Berlin, D)
  • C. Bernardy - Charité Campus Benjamin Franklin, Berlin (Berlin, D)

Hypertonie 2005. 29. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Berlin, 23.-25.11.2005. Düsseldorf, Köln: German Medical Science; 2006. Doc05hochP55

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Veröffentlicht: 8. August 2006

© 2006 Nassar et al.
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Angiotensin-converting enzyme 2 (ACE2) maps to the X chromosome, and a quantitative trait locus (QTL) has been mapped to chromosome X in an experimental cross between the normotensive Wistar Kyoto (WKY) and stroke-prone spontaneously hypertensive (SHRSP) rat. ACE2 cleaves a single residue from angiotensin I (Ang I) to generate Ang-(1-9), and, more importantly, metabolizes the vasoconstrictor Ang II, the main effector of the renin-angiotensin system (RAS), to the vasodilator Ang-(1-7). The role of ACE2 in normal physiology and hypertensive states is largely unknown. Therefore, the aim of our study was to investigate the relationship between renal ACE2 expression and hypertension and to test ACE2 as a candidate gene for blood pressure control in SHRSP. We studied male WKY and SHRSP rats at 16 weeks of age (n=8, respectively). ACE2 mRNA levels in the kidney were measured by Real-time PCR. ACE2 activity was determined with a fluorimetric assay using an ACE2-specific substrate.

Blood pressure was significantly elevated in SHRSP compared to WKY (235±7 vs. 124±6 mmHg, p< 0.0001). ACE2 mRNA expression level were not significantly different (p=0.76) between WKY (100±34%) and SHRSP (106±31%). In accordance with the mRNA expression data, ACE2 activity (micro-molMcAP-OH/mgProtein/h) was also similar in both strains (3.45±0.32 WKY, 3.38±0.30% SHRSP; p=0.65).

Our results show, that renal ACE2 mRNA expression and activity are not altered in hypertensive SHRSP. Moreover, in contrast to previous suggestions, our data indicate that ACE2 may not represent the candidate gene for the blood pressure QTL on rat chromosome X identified in SHRSP.