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| Hypertensive development begins around 5-6 weeks of age, reaching ] pressures between 180 and 200 ] in the adult age phase. Starting between 40 and 50 weeks, SHR develops characteristics of cardiovascular disease, such as ] and ] ] {{ref|conrad1995}}. | Hypertensive development begins around 5-6 weeks of age, reaching ] pressures between 180 and 200 ] in the adult age phase. Starting between 40 and 50 weeks, SHR develops characteristics of cardiovascular disease, such as ] and ] ] {{ref|conrad1995}}. | ||
| == Blood pressure follows the kidney == | |||
| ] a kidney from SHR to a normotensive ] produce increased blood pressure in the recipient. Converesely, transferring a normal Wistar kidney to SHR normalizes blood pressure {{ref|kawabe1978}}. | |||
| == SHR and coping == | == SHR and coping == | ||
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| | id = | | id = | ||
| | url = http://circ.ahajournals.org/cgi/content/full/91/1/161 | | url = http://circ.ahajournals.org/cgi/content/full/91/1/161 | ||
| }} | |||
| *{{note|kawabe1978}}{{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 | |||
| | issue = | |||
| | pages = 886–894 | |||
| | id = | |||
| | url = | |||
| }} | }} | ||
| *{{note|churchill2002}}{{cite journal | *{{note|churchill2002}}{{cite journal | ||
Revision as of 20:31, 13 December 2007
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 follows the kidney
Transplanting a kidney from SHR to a normotensive Wistar rat produce increased blood pressure in the recipient. Converesely, transferring a normal Wistar kidney to SHR normalizes blood pressure .
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.
{{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. (1995). "Myocardial fibrosis and stiffness with hypertrophy and heart failure in the spontaneously hypertensive rat". Circulation. 91: 161–70.
{{cite journal}}: Cite has empty unknown parameter:|month=(help) - 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); line feed character in |title= at position 19 (help)CS1 maint: multiple names: authors list (link)
- 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.
{{cite journal}}: Cite has empty unknown parameter:|month=(help)CS1 maint: multiple names: authors list (link)