This is an old revision of this page, as edited by FrankHansen99 (talk | contribs) at 18:47, 13 December 2007 (→Other uses: deleted superfluous text). The present address (URL) is a permanent link to this revision, which may differ significantly from the current revision.
Revision as of 18:47, 13 December 2007 by FrankHansen99 (talk | contribs) (→Other uses: deleted superfluous text)(diff) ← Previous revision | Latest revision (diff) | Newer revision → (diff)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 . The SHR strain was obtained during the 1960s by Okamoto and colleagues, who started breeding Wistar-Kyoto rats with high blood pressure .
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 .
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 , demonstrating an apithological 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 ischemic stroke and attention-deficit hyperactivity disorder.
See also
References
- Pinto, Y. M., M. Paul, D. Ganten (1998). "Lessons from rat models of hypertension: from Goldblatt to genetic engineering.". Cardiovasc Res. 39: 77–88.
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(help)CS1 maint: multiple names: authors list (link) - Okamoto, A. K. (1963). "Development of a strain of spontaneously hypertensive rat". Jap Circ J. 27: 282–293.
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(help) - Conrad, C. H. (1995). "Myocardial fibrosis and stiffness with hypertrophy and heart failure in the spontaneously hypertensive rat". Circulation. 91: 161–70.
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(help) - Churchill, P. C., W. W. Brooks, J. A. Hayes, S. Sen, K. G. Robinson, O. H. Bing. (2002). "Increased genetic susceptibility to renal damage in the stroke-prone spontaneously hypertensive rat". Kidney Int. 61: 1794–800.
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