Spontaneously hypertensive rat

Spontaneously hypertensive rat (SHR) is an animal model of essential (or primary) hypertension, used to study cardiovascular disease. It is the most studied model of hypertension measured as number of publications ref|pinto1998. The SHR strain was obtained during the 1960s by Okamoto and colleagues, who started breeding Wistar-Kyoto rats with high blood pressure ref|okamoto1963.

Pathophysiology

Hypertensive development begins around 5-6 weeks of age, reaching systolic pressures between 180 and 200 mmHg in the adult age phase. Starting between 40 and 50 weeks, SHR develops characteristics of cardiovascular disease, such as vascular and cardiac hypertrophy ref|conrad1995.

Blood pressure in SHR depends on the kidney

Hypertensive development is somehow connected to the kidney. Transplanting a kidney from SHR to a normotensive Wistar rat increases blood pressure in the recipient. Conversely, transferring a Wistar kidney to SHR normalizes blood pressure in the recipient ref|kawabe1978. This also happens if transplantation takes place at young age before established hypertension in the donors ref|rettig1993, indicating a primary role for the kidney in the development of hypertension in SHR.

SHR and coping

Even though SHR is usually considered to be a purely pathological model, the strain exhibit interesting compensatory abilities. For example, kidneys transplanted from SHR to a hypertensive recipient retain better morphology than kidneys transplanted from Brown Norway ref|churchill2002, demonstrating an apithological [http://www.emrgnc.com.au/apithology.htm] adaptation to high blood pressure.

The stroke prone SHR

Stroke prone SHR (SHR-SP) is a further development of SHR that has even higher blood pressure than SHR and a strong tendency to die from stroke.

Other uses

Spontaneously hypertensive rat is also used as a model of attention-deficit hyperactivity disorder.

ee also

Animal models of ischemic stroke

References

*cite journal
author = Pinto, Y. M., M. Paul, D. Ganten
year = 1998
month =
title = Lessons from rat models of hypertension: from Goldblatt to genetic engineering
journal = Cardiovasc Res
volume = 39
issue =
pages = 77–88
id =
url = http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T14-3T1BDC5-7&_user=596755&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000030718&_version=1&_urlVersion=0&_userid=596755&md5=ad2bad1073fa953f3c4ded636aa26094
doi = 10.1016/S0008-6363(98)00077-7
*cite journal
author = Okamoto, A. K.
year = 1963
month =
title = Development of a strain of spontaneously hypertensive rat
journal = Jap Circ J
volume = 27
issue =
pages = 282–293
id =
url =
*cite journal
author = Conrad, C. H.
year = 1995
month =
title = Myocardial fibrosis and stiffness with hypertrophy and heart failure in the spontaneously hypertensive rat
journal = Circulation
volume = 91
issue =
pages = 161–70
id =
url = http://circ.ahajournals.org/cgi/content/full/91/1/161
pmid = 7805198
*cite journal
author = Kawabe, K., T. X. Watanabe, K. Shiono, H. Sokabe.
year = 1978
month =
title = Influence on blood pressure of renal isografts between spontaneously hypertensive and normotensive rats, utilizing the F1 hybrids
journal = Jpn Heart J
volume = 19
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pages = 886–894
id =
url =
*cite journal
author = Rettig, R.
year = 1993
month =
title = Does the kidney play a role in the aetiology of primary hypertension? Evidence from renal transplantation studies in rats and humans
journal = J Hum Hypertens
volume = 7
issue =
pages = 177–180
id =
url =
*cite journal
author = Churchill, P. C., W. W. Brooks, J. A. Hayes, S. Sen, K. G. Robinson, O. H. Bing.
year = 2002
month =
title = Increased genetic susceptibility to renal damage in the stroke-prone spontaneously hypertensive rat
journal = Kidney Int
volume = 61
issue =
pages = 1794–800
id =
url = http://www.nature.com/ki/journal/v61/n5/abs/4492945a.html;jsessionid=5D5701F05F69F743E88D311569A95301
doi = 10.1046/j.1523-1755.2002.00321.x