Cardiovascular end-organ damage in Ren-2 transgenic rats compared to spontaneously hypertensive rats.
To compare hypertensive end-organ damage in two genetic forms of hypertension we assessed cardiovascular function in two rat strains of genetic hypertension: transgenic rats overexpressing the mouse Ren-2 gene [(TGR(mREN2)27]) and blood pressure matched spontaneously hypertensive rats (SHR). Despite similarly elevated blood pressure, systolic dp/dt (mmHg/s) was more impaired in transgenic rats (3099 +/- 446) than in SHR (3571 +/- 272) and normals (4342 +/- 119; P < 0.05). Left ventricular weight (mg/g body weight) increased more in the transgenic rats (40 +/- 3) than in SHR (31 +/- 2) and normals (26 +/- 2). Endothelium-dependent relaxation was significantly decreased only in the transgenic rats. This study shows significantly more cardiac and endothelial dysfunction in transgenic, hypertensive TGR (mREN2)27 than in age and blood pressure matched SHR. This supports the hypothesis that chronic activation of the renin-angiotensin system significantly contributes to hypertensive end-organ damage.
Pinto
Y M
YM
Department of Clinical Pharmacology, University of Groningen, The Netherlands.
Buikema
H
H
van Gilst
W H
WH
Scholtens
E
E
van Geel
P P
PP
de Graeff
P A
PA
Wagner
J
J
Paul
M
M
D000818:Animals; D030801:Animals, Genetically Modified; D004195:Disease Models, Animal; D004727:Endothelium / Q000502:physiology; D006973:Hypertension / Q000235:genetics / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D051379:Mice; D009206:Myocardium / Q000473:pathology; D007703:Peptidyl-Dipeptidase A / Q000097:blood / Q000378:metabolism; D012333:RNA, Messenger; D051381:Rats; D011918:Rats, Inbred SHR; D017207:Rats, Sprague-Dawley; D017208:Rats, Wistar; D012083:Renin / Q000097:blood / Q000235:genetics*; D012084:Renin-Angiotensin System / Q000235:genetics / Q000502:physiology*
D012333:RNA, Messenger; D007703:Peptidyl-Dipeptidase A; D012083:Renin