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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 .

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 . This also happens if transplantation takes place at young age before established hypertension in the donors , 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 , 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.

Attention Deficit Hyperactivity Disorder

The Spontaneously Hypertensive Rat is also used as a model of attention-deficit hyperactivity disorder. To avoid confounds associated with hypertension, when using the animal as a model of ADHD, research starts around post-natal day (PND) 28 (when the animal is four weeks old).

Reference strain

The reference strain (of which the SHR is compared against) is the Sprague-Dawley

Controversy exists on how useful the model is for relating findings to humans.

Other uses

The Spontaneous Hypertensive Rat is also a model of anxiety.

See also

Animal models of ischemic stroke

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. doi:10.1016/S0008-6363(98)00077-7. {{cite journal}}: Cite has empty unknown parameter: |month= (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. {{cite journal}}: Cite has empty unknown parameter: |month= (help)
• Conrad, C. H. (January 1, 1995). "Myocardial fibrosis and stiffness with hypertrophy and heart failure in the spontaneously hypertensive rat". Circulation. 91 (1): 161–70. PMID 7805198.
• Kawabe, K., T. X. Watanabe, K. Shiono, H. Sokabe. (1978). "Influence on blood pressure of renal isografts between spontaneously hypertensive and normotensive rats, utilizing the F1 hybrids". Jpn Heart J. 19: 886–894. {{cite journal}}: Cite has empty unknown parameter: |month= (help)CS1 maint: multiple names: authors list (link)
• Rettig, R. (1993). "Does the kidney play a role in the aetiology of primary hypertension? Evidence from renal transplantation studies in rats and humans". J Hum Hypertens. 7: 177–180. {{cite journal}}: Cite has empty unknown parameter: |month= (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. doi:10.1046/j.1523-1755.2002.00321.x. {{cite journal}}: Cite has empty unknown parameter: |month= (help)CS1 maint: multiple names: authors list (link)

• Animal testing