(Hypertension. 1995;26:998-1002.)
© 1995 American Heart Association, Inc.
Articles |
From the Cardiovascular Research Center, Massachusetts General HospitalEast (G.K., E.S.W., D.M.B., H.J.J.), Charlestown; the Falk Cardiovascular Research Center, Stanford University School of Medicine (M.H., VJ.D.), Stanford, Calif; and the Département de Biologie Moléculaire, Université Libre de Bruxelles (C.S.), Rhode-St-Genèse, Belgium.
Correspondence to Howard J. Jacob, PhD, Cardiovascular Research Center, Mail Code 1494201, Massachusetts General HospitalEast, 149 13th St, Charlestown, MA 02129-2060. E-mail jacob@helix.mgh.harvard.edu.
Abstract The renin-angiotensin system plays an important role in blood pressure homeostasis, but the contribution of the type 2 angiotensin II receptor (AT2R) is still unclear. The reports that the AT2R gene has been mapped to the X chromosome in human and rat and the previous report of a gene, Bp3, on the X chromosome responsible for an increase in blood pressure have suggested that the rat AT2R gene (Agtr2) could be this gene. To elucidate whether Agtr2 is Bp3, Agtr2 was cloned. A simple sequence repeat in the 3'-flanking region of this gene was identified and used as a genetic marker to map Agtr2 to the X chromosome at 18.1 cM distal to the androgen receptor locus. This map position is outside the confidence interval reported for Bp3, demonstrating that Agtr2 cannot be Bp3. However, these data will enhance the research into the AT2R biology as well as the study of the X chromosome.
Key Words: receptor, angiotensin rats cloning, molecular
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