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(Hypertension. 1999;33:256-260.)
© 1999 American Heart Association, Inc.

Scientific Contributions

Effect of Chromosome 19 Transfer on Blood Pressure in the Spontaneously Hypertensive Rat

Elizabeth St. Lezin; Lei Zhang; Ying Yang; Jia-Ming Wang; Ning Wang; Nianing Qi; J. Sanford Steadman; Weizhong Liu; Vladimir Kren; Vaclav Zidek; Drahomira Krenova; Paul C. Churchill; Monique C. Churchill; Michal Pravenec

From the Department of Laboratory Medicine, University of California, San Francisco, Calif (E.S.L., L.Z., Y.Y., J-M.W., N.W., N.Q., J.S.S., W.L.); Institute of Biology and Medical Genetics, 1st Medical Faculty, Charles University, Prague, Czech Republic (V.K., D.K., M.P.); Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic (V.K., V.Z., M.P.); and Department of Physiology, Wayne State University School of Medicine, Detroit, Mich (P.C.C., M.C.C.).

Correspondence to Elizabeth St. Lezin, MD, Department of Laboratory Medicine, UCSF/Mt. Zion Medical Center, 1600 Divisadero St, San Francisco, CA 94143-1613. E-mail stlezin{at}pangloss.ucsf.edu

Abstract—Linkage studies in the spontaneously hypertensive rat (SHR) have suggested that a gene or genes regulating blood pressure may exist on rat chromosome 19 in the vicinity of the angiotensinogen gene. To test this hypothesis, we measured blood pressure in SHR progenitor and congenic strains that are genetically identical except for a segment of chromosome 19 containing the angiotensinogen gene transferred from the normotensive Brown Norway (BN) strain. Transfer of this segment of chromosome 19 from the BN strain onto the genetic background of the SHR induced significant decreases in systolic and diastolic blood pressures in the recipient SHR chromosome 19 congenic strain. To test for differences in angiotensinogen gene expression between the congenic and progenitor strains, we measured angiotensinogen mRNA levels in a variety of tissues, including aorta, brain, kidney, and liver. We found no differences between the progenitor and congenic strains in the angiotensinogen coding sequence or in angiotensinogen expression that would account for the blood pressure differences between the strains. In addition, no significant differences in plasma levels of angiotensinogen or plasma renin activity were detected between the 2 strains. Thus, transfer of a segment of chromosome 19 containing angiotensinogen from the BN rat into the SHR induces a decrease in blood pressure without inducing any major changes in plasma angiotensinogen levels or plasma renin activity. These results indicate that the differential chromosome segment trapped in the SHR chromosome 19 congenic strain contains a quantitative trait locus that influences blood pressure in the SHR but that this blood pressure effect is not explained by differences in plasma angiotensinogen levels or angiotensinogen expression.

Key Words: hypertension, experimental • angiotensinogen • genetics • blood pressure • rats

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