| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Hypertension, Vol 19, 419-424, Copyright © 1992 by American Heart Association
E St. Lezin, L Simonet, M Pravenec and TW Kurtz
The spontaneously hypertensive rat and the Dahl salt-sensitive rat are the
most widely studied genetic models of hypertension. Many investigators have
attempted to study the pathogenesis of hypertension by comparing these
strains with their respective normotensive "controls," the Wistar-Kyoto rat
and the Dahl salt-resistant rat. However, the genetic relation between each
of these hypertensive strains and its corresponding normotensive control
has never been clearly defined. Based on an analysis of DNA "fingerprint"
patterns generated with six multilocus probes, we found that the
spontaneously hypertensive rat (Charles River Laboratories, Inc.) is
genetically quite different from its normotensive Wistar-Kyoto control:
these strains only share approximately 50% of their DNA fingerprint bands
in common. The inbred Dahl salt-sensitive rat (SS/Jr strain) (Harlan
Sprague Dawley, Inc.) and the Dahl salt-resistant rat (SR/Jr strain) share
approximately 80% of their DNA fingerprint bands in common. To the extent
that the genes identified by DNA fingerprint analysis are representative of
loci dispersed throughout the rodent genome, the current findings provide
evidence of extensive genetic polymorphism between these commonly used
hypertensive strains and their corresponding normotensive controls,
particularly in the spontaneously hypertensive rat model. These findings,
together with the fact that an enormous number of biochemical and
physiological differences have been reported between these hypertensive and
normotensive strains, suggest that continued comparison of spontaneously
hypertensive rats with Wistar-Kyoto rats or Dahl salt-sensitive with
salt-resistant rats will have limited value for investigating the
pathogenesis of hypertension.
ARTICLES
Hypertensive strains and normotensive 'control' strains. How closely are they related?
Department of Laboratory Medicine, University of California, San Francisco 94143-0134.
This article has been cited by other articles:
![]() |
F. Feihl, L. Liaudet, B. I. Levy, and B. Waeber Hypertension and microvascular remodelling Cardiovasc Res, May 1, 2008; 78(2): 274 - 285. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. P. Didion, M. J. Ryan, G. L. Baumbach, C. D. Sigmund, and F. M. Faraci Superoxide contributes to vascular dysfunction in mice that express human renin and angiotensinogen Am J Physiol Heart Circ Physiol, October 1, 2002; 283(4): H1569 - H1576. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. E. Magyar, Y. Zhang, N.-H. Holstein-Rathlou, and A. A. McDonough Proximal tubule Na transporter responses are the same during acute and chronic hypertension Am J Physiol Renal Physiol, August 1, 2000; 279(2): F358 - F369. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. P. Didion, C. D. Sigmund, F. M. Faraci, and Z. S. Katusic Impaired Endothelial Function in Transgenic Mice Expressing Both Human Renin and Human Angiotensinogen • Editorial Comment Stroke, March 1, 2000; 31(3): 760 - 765. [Abstract] [Full Text] [PDF] |
||||
![]() |
F. M. Faraci and C. D. Sigmund Vascular Biology in Genetically Altered Mice : Smaller Vessels, Bigger Insight Circ. Res., December 3, 1999; 85(12): 1214 - 1225. [Full Text] [PDF] |
||||
![]() |
J. Zicha and J. Kunes Ontogenetic Aspects of Hypertension Development: Analysis in the Rat Physiol Rev, October 1, 1999; 79(4): 1227 - 1282. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. A Doggrell and L. Brown Rat models of hypertension, cardiac hypertrophy and failure Cardiovasc Res, July 1, 1998; 39(1): 89 - 105. [Full Text] [PDF] |
||||
![]() |
W. R. Dunn and S. M. Gardiner Structural and Functional Properties of Isolated, Pressurized, Mesenteric Resistance Arteries From a Vasopressin-Deficient Rat Model of Genetic Hypertension Hypertension, September 1, 1995; 26(3): 390 - 396. [Abstract] [Full Text] |
||||
![]() |
A. Koller and A. Huang Shear Stress–Induced Dilation Is Attenuated in Skeletal Muscle Arterioles of Hypertensive Rats Hypertension, April 1, 1995; 25(4): 758 - 763. [Abstract] [Full Text] |
||||
![]() |
K. Amann, H. Gharehbaghi, S. Stephan, and G. Mall Hypertrophy and Hyperplasia of Smooth Muscle Cells of Small Intramyocardial Arteries in Spontaneously Hypertensive Rats Hypertension, January 1, 1995; 25(1): 124 - 131. [Abstract] [Full Text] |
||||
|
Hypertension Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1992 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |