Hypertension, Vol 19, 687-691, Copyright © 1992 by American Heart Association
KF Hilgers, J Peters, R Veelken, M Sommer, G Rupprecht, D Ganten, FC Luft and JF Mann
Rats harboring the mouse Ren-2 transgene develop hypertension despite low
levels of plasma renin activity. We tested the hypothesis that these rats
exhibit an increase in vascular angiotensin formation caused by the
presence of the transgene. We measured the release of angiotensins I and II
from isolated perfused hindquarters by high- performance liquid
chromatography and radioimmunoassay. Female rats heterozygous for the
transgene had significantly elevated mean arterial pressure compared with
control rats (189.3 +/- 9.5 versus 110.0 +/- 5.4 mm Hg, p less than 0.05).
Plasma angiotensin II was significantly decreased in transgenic rats.
Transgenic rat hindquarters released more angiotensin I (121 +/- 37 versus
39 +/- 12 fmol/30 min, n = 7 each) and more angiotensin II (210 +/- 21
versus 62 +/- 12 fmol/30 min, p less than 0.05, n = 7 each) than control
rat hindquarters. Captopril increased angiotensin I release and decreased
angiotensin II values in both transgenic and control rat hindquarters.
Bilateral nephrectomy 24 hours before hindquarter perfusion greatly reduced
angiotensin release from control rat hindquarters but not from transgenic
rat hind limbs. We also tested for the presence of Ren-2 messenger RNA in
mesenteric and aortic tissue by RNase protection assay and Northern blot
analysis. We found that Ren-2 messenger RNA was present in mesenteric and
aortic tissue of transgenic but not of control rats. We conclude that the
Ren- 2 transgene is expressed in vascular tissue of transgenic rats and may
be responsible for substantial increases in vascular angiotensin formation.
ARTICLES
Increased vascular angiotensin formation in female rats harboring the mouse Ren-2 gene
Department of Medicine-Nephrology, University of Erlangen-Nurnberg, FRG.
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