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(Hypertension. 1998;31:373.)
© 1998 American Heart Association, Inc.

Scientific Contributions

Effect of Renin Gene Transfer on Blood Pressure in the Spontaneously Hypertensive Rat

Elizabeth St. Lezin; Weizhong Liu; Ning Wang; Jia-Ming Wang; Vladimir Kren; Vaclav Zidek; Miroslava Zdobinska; Drahomira Krenova; Anita Bottger; Bert F. M. van Zutphen; Michal Pravenec

From the Department of Laboratory Medicine, University of California, San Francisco, Calif. (E.S., W. L., N. W., J.-M. W.); the Institute of Biology, 1st Medical Faculty, Charles University, Prague, Czech Republic (V.K., D.K., M.P.); the Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic (V.K., V.Z., M.Z., M.P.); and the Department of Laboratory Animal Science, Veterinary Faculty, University of Utrecht, Utrecht, Netherlands (A.B., B.F.M. v Z.)

Correspondence to Elizabeth St. Lezin, MD, Department of Laboratory Medicine, UCSF/Mt. Zion Medical Center 1613, PO Box 7921, San Francisco, CA 94120. E-mail stlezin{at}pangloss.ucsf.edu

To investigate whether molecular variation in the renin gene contributes to the greater blood pressure of spontaneously hypertensive rats (SHR) versus normotensive Brown Norway (BN) rats, we measured blood pressure in an SHR progenitor strain and an SHR congenic strain that are genetically identical except at the renin gene and an associated segment of chromosome 13 transferred from the BN strain. Backcross breeding and molecular selection at the renin locus were used to create the SHR congenic strain (designated SHR.BN-Ren) that carries the renin gene transferred from the normotensive BN strain. We found that transfer of the renin gene from the BN strain onto the genetic background of the SHR did not decrease blood pressure in rats fed either a normal or high-salt diet. In fact, the systolic blood pressures of the SHR congenic rats tended to be slightly greater than the systolic blood pressures of the SHR progenitor rats. However, the congenic strain exhibited lower serum high-density lipoprotein cholesterol, and greater levels of total cholesterol, very-low-density lipoprotein, and intermediate-density lipoprotein cholesterol during administration of a high-fat, high-cholesterol diet. These findings demonstrate that (1) under the environmental circumstances of the current study, the greater blood pressure of SHR versus BN rats cannot be explained by strain differences in the renin gene and (2) a quantitative trait locus affecting lipid metabolism exists on chromosome 13 within the transferred chromosome segment. The SHR.BN-Ren congenic strain may provide a useful new animal model for studying the interaction between high blood pressure and dyslipidemia in cardiovascular disease.

Key Words: hypertension • cholesterol • genetics • congenic • quantitative trait locus • renin • rat

Abbreviations: BN = Brown Norway • HDL = high-density lipoprotein • IDL = intermediate-density lipoprotein • LDL = low-density lipoprotein • PCR = polymerase chain reaction • QTL = quantitative trait locus • RI = recombinant inbred • SHR = spontaneously hypertensive rat(s) • VLDL = very-low-density lipoprotein

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