1. ^* Centre d'Etude du Polymorphisme Humain, 27 rue Juliette Dodu, 75010 Paris, France
2. ^† IRIBNH, Campus Erasme, Brussels 1070, Belgium
3. ^‡ Department of Cellular and Molecular Physiology, Harvard Medical School, Boston, Massachusetts 02115, USA
4. ^§ German Institute for High Blood Pressure, and Department of Pharmacology, University of Heidelberg, D-6900 Heidelberg, Germany
5. Institute of Laboratory Animals, Faculty of Medicine, Kyoto University, Kyoto 606, Japan
6. ^¶INSERM U. 36, Laboratoire de Médicine Expérimental, Collége de France, Paris 75005, France
7. ^£ Department of Human Genetics, University of Utah, Salt Lake City, Utah 84132, USA
8. ^** Laboratoire de Physiologie, Université Claude Bernard, Lyon 69373, France
9. ^†† Centre for Molecular Medicine, Berlin-Buch 0-1115, Germany
10. ^‡‡ Genmark Inc., 417 Wakara Way, Salt Lake City, Utah 84108, USA
11. ^§§ To whom correspondence should be addressed.

Abstract

The spontaneously hypertensive rat and the stroke-prone spontaneously hypertensive rat are useful models for human hypertension. In these strains hypertension is a polygenic trait, in which both autosomal and sex-linked genes can influence blood pressure^1–7. Linkage studies in crosses between the stroke-prone spontaneously hypertensive rat and the normotensive control strain Wistar-Kyoto have led to the localization of two genes, BP/SP-1 and BP/SP-2, that contribute significantly to blood pressure variation in the F₂ population. BP/SP-1and BP/SP-2 were assigned to rat chromosomes 10 and X, respectively. Comparison of the human and rat genetic maps indicates that BP/SP-1 could reside on human chromosome 17q in a region that also contains the angiotensin l-converting enzyme gene (ACE)⁸. This encodes a key enzyme of the renin-angiotensin system⁹, and is therefore a candidate gene in primary hypertension. A rat microsatellite marker of ACE was mapped to rat chromosome 10 within the region containing BP/SP-1.