Cardiovascular end-organ damage in Ren-2 transgenic rats compared to spontaneously hypertensive rats

J Mol Med (1997) 75:371–377

© Springer-Verlag 1997

O R I G I NA L A RT I C L E

&roles:Yigal M. Pinto · Hendrik Buikema · Wiek H. van Gilst Egbert Scholtens · Peter-Paul van Geel Pieter A. de Graeff · Jürgen Wagner · Martin Paul

Cardiovascular end-organ damage in Ren-2 transgenic rats compared to spontaneously hypertensive rats &misc:Received: 25 November 1996 / Accepted: 18 January 1997

YIGAL M. PINTO studied medicine at the University of Groningen, Netherlands, where he is presently a resident in cardiology. He also trained at the Free University of Berlin via an ICIN fellowship. His major research interests include pathophysiological role of the renin-angiotensin system, transgenic rat models, and somatic gene transfer.

MARTIN PAUL studied medicine at the University of Heidelberg, Germany, and trained at the University of California, San Diego, Heidelberg University and Harvard University, USA. He is presently chairman of the Department of Clinical Pharmacology and Toxicology and Director of the Cardiovascular Research Center at the Free University of Berlin. His research interests include peptidergic systems and gene transfer into the cardiovascular system.

Y.M. Pinto Department of Clinical Pharmacology, University of Groningen, and Freie Universität Berlin, Universitätsklinikum Benjamin Franklin, Department of Clinical Pharmacology and Toxicology, Hindenburgdamm 30, D-12200 Berlin, Germany H. Buikema · W.H. van Gilst · E. Scholtens P.-P. van Geel · P.A. de Graeff Department of Clinical Pharmacology, University of Groningen, Groningen, The Netherlands J. Wagner · M. Paul Freie Universität Berlin, Universitätsklinikum Benjamin Franklin, Department of Clinical Pharmacology and Toxicology, Hindenburgdamm 30, D-12200 Berlin, Germany&/fn-block:

&p.1:Abstract 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