Cosegregation of the renin allele of the spontaneously hypertensive rat with an increase in blood pressure.

T W Kurtz; L Simonet; P M Kabra; S Wolfe; L Chan; B L Hjelle

doi:10.1172/JCI114572

Department of Laboratory Medicine, University of California, San Francisco 94143.

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Department of Laboratory Medicine, University of California, San Francisco 94143.

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Department of Laboratory Medicine, University of California, San Francisco 94143.

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Department of Laboratory Medicine, University of California, San Francisco 94143.

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Department of Laboratory Medicine, University of California, San Francisco 94143.

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Department of Laboratory Medicine, University of California, San Francisco 94143.

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Published in Volume 85, Issue 4 on April 1, 1990
J Clin Invest. 1990;85(4):1328–1332. https://doi.org/10.1172/JCI114572.
© 1990 The American Society for Clinical Investigation

Published April 1, 1990 - Version history

The spontaneously hypertensive rat (SHR) exhibits alterations in the renin-angiotensin-aldosterone system which are similar to those that characterize patients with "nonmodulating" hypertension, a common and highly heritable form of essential hypertension. Accordingly, we determined whether the inheritance of a DNA restriction fragment length polymorphism (RFLP) marking the renin gene of the SHR was associated with greater blood pressure than inheritance of a RFLP marking the renin gene of a normotensive control rat. In an F2 population derived from inbred SHR and inbred normotensive Lewis rats, we found the blood pressure in rats that inherited a single SHR renin allele to be significantly greater than that in rats that inherited only the Lewis renin allele. To the extent that the SHR provides a suitable model of "nonmodulating" hypertension, these findings raise the possibility that a structural alteration in the renin gene, or a closely linked gene, may be a pathogenetic determinant of increased blood pressure in one of the most common forms of essential hypertension in humans.

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