scholarly journals High-Resolution Identity by Descent Mapping Uncovers the Genetic Basis for Blood Pressure Differences Between Spontaneously Hypertensive Rat Lines

2011 ◽  
Vol 4 (3) ◽  
pp. 223-231 ◽  
Author(s):  
Rebecca Bell ◽  
Stacy M. Herring ◽  
Nisha Gokul ◽  
Monique Monita ◽  
Megan L. Grove ◽  
...  
Keyword(s):  
Blood Pressure ◽  
High Resolution ◽  
Genetic Basis ◽  
Spontaneously Hypertensive Rat ◽  
Identity By Descent ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
Resolution Identity

scholarly journals Genetics of hypertension: an assessment of progress in the spontaneously hypertensive rat

2017 ◽  
Vol 49 (11) ◽  
pp. 601-617 ◽  
Author(s):  
Peter A. Doris
Keyword(s):  
Blood Pressure ◽  
Genetic Basis ◽  
Spontaneously Hypertensive Rat ◽  
Model Organism ◽  
Blood Pressure Elevation ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
Wistar Strain ◽  
Genome Wide ◽  
Common Genetic Variants

The application of gene mapping methods to uncover the genetic basis of hypertension in the inbred spontaneously hypertensive rat (SHR) began over 25 yr ago. This animal provides a useful model of genetic high blood pressure, and some of its features are described. In particular, it appears to be a polygenic model of disease, and polygenes participate in human hypertension genetic risk. The SHR hypertension alleles were fixed rapidly by selective breeding in just a few generations and so are presumably common genetic variants present in the outbred Wistar strain from which SHR was created. This review provides a background to the origins and genesis of this rat line. It considers its usefulness as a model organism for a common cardiovascular disease. The progress and obstacles facing mapping are considered in depth, as are the emergence and application of other genome-wide genetic discovery approaches that have been applied to investigate this model. Candidate genes, their identification, and the evidence to support their potential role in blood pressure elevation are considered. The review assesses the progress that has arisen from this work has been limited. Consideration is given to some of the factors that have impeded progress, and prospects for advancing understanding of the genetic basis of hypertension in this model are discussed.

Hypoxic moderation of systemic hypertension in the spontaneously hypertensive rat

1987 ◽  
Vol 252 (3) ◽  
pp. R554-R561 ◽  
Author(s):  
W. N. Henley ◽  
A. Tucker
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rat ◽  
Metabolic Adaptation ◽  
Systemic Hypertension ◽  
Thyroid Status ◽  
Blood Pressure Elevation ◽  
Spontaneously Hypertensive ◽  
Moderate Hypobaric Hypoxia ◽  
Hypertensive Rat ◽  
Wistar Kyoto

The mechanism by which chronic, moderate, hypobaric hypoxia attenuates systemic systolic blood pressure (SBP) in the spontaneously hypertensive rat (SHR) was investigated in a three-part study. In experiment 1, 10 wk of hypoxia (3,658 m altitude) commencing in 7-wk-old rats was partially effective in preventing the rise in SBP [hypoxic SHR (SHR-H) 154 mmHg vs. normoxic SHR (SHR-N) 180 mmHg; P less than 0.01]. When hypoxia was initiated in 5-wk-old SHR (experiments 2 and 3), protection against hypertension was nearly complete (experiment 2: SHR-H 122 mmHg vs. SHR-N 175 mmHg; P less than 0.001; experiment 3: 135 vs. 152 mmHg, respectively; P less than 0.05). Elevations in O2 consumption (VO2) and rectal temperature (Tre) in SHR vs. normotensive [Wistar-Kyoto (WKY)] rats provided evidence that the SHR is a hypermetabolic animal. Thyroid hormonal indices suggested that SHR changed from a low to high thyroid status at a time that rapid blood pressure elevation occurred; however, hypoxia did not influence thyroid status. Acute, significant decrements in VO2 and Tre in SHR-H (experiments 2 and 3) accompanied the attenuation of SBP by hypoxia, whereas large decrements in VO2 and SBP did not occur in hypoxic WKY. Timely administration of moderate hypoxia protects against the development of hypertension in the SHR. This protection may relate to a metabolic adaptation made by the hypoxic SHR.

Sodium–Proton (Na+/H+) Exchange Inhibition Increases Blood Pressure in Spontaneously Hypertensive Rat

1994 ◽  
Vol 308 (3) ◽  
pp. 145-151 ◽  
Author(s):  
Yiu-Fai Chen ◽  
Ren-Hui Yang ◽  
Qing-Cheng Meng ◽  
Edward J. Cragoe ◽  
Suzanne Oparil
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rat ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat
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