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Strain: SHRSP

Symbol: SHRSP
Strain: SHRSP
Full Name: Spontaneously Hypertensive Rat, Stroke Prone
RGD ID: 61010
Citation ID: RRID:RGD_61010
Ontology ID: RS:0000759
Also Known As: MDC-01-80
Type: inbred
Available Source: Not Available
Origination: Iffa Credo, L'arbresle, France, Max-Delbruck-Center for Molecular Medicine, Berlin-Buch
Description: The A1-sb and A3 substrains of SHR which had been bred as parallel lines from F20 to F36 were crossed (?) and further inbred with selection of offspring of parents that died of stroke (Okamoto et al 1974, 1986, Yamori 1984). To NIH in 1976, and designated SHRSP/A3N. Pathophysiology reviewed by Volpe and Rubattu (1994).
Genetic Markers: c
Coat Color: Albino,
Inbred Generations: F59.
Last Known Status: Unknown

Mutant Strains
SHRSP/Ta




Disease Annotations     Click to see Annotation Detail View
hypertension  (IAGP)
Stroke  (IAGP)

Phenotype Annotations     Click to see Annotation Detail View

Phenotype Values via PhenoMiner     Click to see Annotation Detail View
Options:  View chart  |  Download data table  |  View expanded data table


References

References - curated
# Reference Title Reference Citation
1. Mutant animal models of stroke and gene expression: the stroke-prone spontaneously hypertensive rat. Carswell HV, etal., Methods Mol Med 2005;104:49-74.
2. Cd36 and molecular mechanisms of insulin resistance in the stroke-prone spontaneously hypertensive rat. Collison M, etal., Diabetes 2000 Dec;49(12):2222-6.
3. Inbred Strains Festing, MFW, Inbred Strains, The Laboratory Rat, 1979, Baker HK, Lindsey JR, Weisbroth SH, 55-72, Academic Press
4. Update to previous Strain Data Festing, MFW, Personal Communication Update, Feb-2000
5. Contribution of Genetic Factors to Renal Lesions in the Stroke-Prone Spontaneously Hypertensive Rat. Gigante B, etal., Hypertension 2003 Oct;42(4):702-6. Epub 2003 Jul 21.
6. Chromosomal mapping of two genetic loci associated with blood-pressure regulation in hereditary hypertensive rats Hilbert P, etal., Nature 1991 Oct 10;353(6344):521-9
7. Genetic mapping of a gene causing hypertension in the stroke-prone spontaneously hypertensive rat. Jacob HJ, etal., Cell 1991 Oct 4;67(1):213-24
8. Sensitivity to cerebral ischaemic insult in a rat model of stroke is determined by a single genetic locus. Jeffs B, etal., Nat Genet 1997 Aug;16(4):364-7
9. Genome-wide searches for blood pressure quantitative trait loci in the stroke-prone spontaneously hypertensive rat of a Japanese colony. Kato N, etal., J Hypertens 2003 Feb;21(2):295-303.
10. Lacidipine prevents endothelial dysfunction in salt-loaded stroke-prone hypertensive rats. Krenek P, etal., Hypertension 2001 Apr;37(4):1124-8.
11. Evidence for primary genetic determination of heart rate regulation: chromosomal mapping of a genetic locus in the rat. Kreutz R, etal., Circulation 1997 Aug 19;96(4):1078-81.
12. Dissection of a quantitative trait locus for genetic hypertension on rat chromosome 10. Kreutz R, etal., Proc Natl Acad Sci U S A 1995 Sep 12;92(19):8778-82.
13. Molecular genetics of the SA-gene: cosegregation with hypertension and mapping to rat chromosome 1. Lindpaintner K, etal., J Hypertens 1993 Jan;11(1):19-23
14. Prevention of nephrosclerosis and cardiac hypertrophy by captopril treatment of spontaneously hypertensive rats. Ohashi H, etal., Jpn Circ J. 1986 Feb;50(2):140-6.
15. RGD Strain RSO annotation pipeline RGD Automated Pipelines
16. Chromosomal mapping of quantitative trait loci contributing to stroke in a rat model of complex human disease Rubattu S, etal., Nat Genet 1996 Aug;13(4):429-34
17. SNP and haplotype mapping for genetic analysis in the rat. Saar K, etal., Nat Genet. 2008 May;40(5):560-6.
18. A high density integrated genetic linkage and radiation hybrid map of the laboratory rat Steen RG, Kwitek-Black AE, etal., Genome Research, 1999, 6:1-8

Region

Strain QTL Data
Symbol Name Trait
Bp1 Blood pressure QTL 1 arterial blood pressure trait   (VT:2000000)    
Bp2 Blood pressure QTL 2 arterial blood pressure trait   (VT:2000000)    
Bp28 Blood pressure QTL 28 arterial blood pressure trait   (VT:2000000)    
Bp3 Blood pressure QTL 3 arterial blood pressure trait   (VT:2000000)    
Bp4 Blood pressure QTL 4 arterial blood pressure trait   (VT:2000000)    
Bp49 Blood pressure QTL 49 cerebrum integrity trait   (VT:0010549)    
Hrtrt17 Heart rate QTL 17 heart pumping trait   (VT:2000009)    
Rends2 Renal damage susceptibility QTL 2 kidney blood vessel morphology trait   (VT:0000530)    
Rends3 Renal damage susceptibility QTL 3 kidney blood vessel morphology trait   (VT:0000530)    
Rends4 Renal damage susceptibility QTL 4 kidney blood vessel morphology trait   (VT:0000530)    

Additional Information

RGD Curation Notes
Note Type Note Reference
strain_characteristics Stroke in these rats is affected by both genetic and environmental factors. Hypertension, vascular wall changes, and salt metabolism as well as a reduction in cerebral blood flow are important systemic and local factors in the stroke. Stroke is prevented by antihypertensive agents and the incidence can be modified by diet, being reduced by the inclusion of fish and vegetable oils. Excessive salt intake increases hypertension and its complications. A high protein diet attenuated the development of severe hypertension, and counteracted the adverse effect of salt. High relative heart weight in 10-week old males (23/23) (Tanase et al 1982). Liver gangliosides are of the b-type (cf WKAH) (Kasai et al 1993). There was no evidence for co-segregation between blood pressure and the angiotensinogen locus, or any other phenotypic parameter in crosses involving WKY (Hubner et al, 1994, 1995). 1004
strain_characteristics Stroke in these rats is affected by both genetic and environmental factors. Hypertension, vascular wall changes, and salt metabolism as well as a reduction in cerebral blood flow are important systemic and local factors in the stroke. Stroke is prevented by antihypertensive agents and the incidence can be modified by diet, being reduced by the inclusion of fish and vegetable oils. Excessive salt intake increases hypertension and its complications. A high protein diet attenuated the development of severe hypertension, and counteracted the adverse effect of salt. High relative heart weight in 10-week old males (23/23) (Tanase et al 1982). Liver gangliosides are of the b-type (cf WKAH) (Kasai et al 1993). There was no evidence for co-segregation between blood pressure and the angiotensinogen locus, or any other phenotypic parameter in crosses involving WKY (Hubner et al, 1994, 1995). 634612
strain_characteristics Stroke in these rats is affected by both genetic and environmental factors. Hypertension, vascular wall changes, and salt metabolism as well as a reduction in cerebral blood flow are important systemic and local factors in the stroke. Stroke is prevented 1004
strain_characteristics Stroke in these rats is affected by both genetic and environmental factors. Hypertension, vascular wall changes, and salt metabolism as well as a reduction in cerebral blood flow are important systemic and local factors in the stroke. Stroke is prevented 634612
strain_drgs_chems Lacidipine treatment prevented the salt-dependent functional and structural alterations of the aorta, including the overexpression of the preproendothelin-1 gene, and increased endothelial NO synthase mRNA levels in aortic tissue. This effect may contribute to its beneficial effect against end-organ damage and stroke. 68703
strain_phys_biochem High blood pressure (1/23), reaching 187_2.2 (SEM) mmHg at 10 weeks of age (Tanase et al 1982). The hypertension has been extensively reviewed by Yamori (1984) as follows: Cerebral hemorrhage or infarction in 82% of males over 100 days of age and 58% of females over 150 days of age. The main sites are the anteriomedial and occipital cortex, and the basal ganglia. They have a higher blood pressure (by 40-50 mmHg) than SHR, and in both strains the blood pressure is maintained by higher peripheral vascular resistance which at first is due to neurogenic vasoconstriction. Membrane changes may be involved. Regional cerebral blood flow is reduced, especially in areas of the brain fed by recurrent branches. Body weight is lower than in SHR. Signs of stroke include piloerection, hyperkinesis, hyperirritability, aggressiveness and motion disturbance. 1004
strain_phys_biochem High blood pressure (1/23), reaching 187_2.2 (SEM) mmHg at 10 weeks of age (Tanase et al 1982). The hypertension has been extensively reviewed by Yamori (1984) as follows: Cerebral hemorrhage or infarction in 82% of males over 100 days of age and 58% of females over 150 days of age. The main sites are the anteriomedial and occipital cortex, and the basal ganglia. They have a higher blood pressure (by 40-50 mmHg) than SHR, and in both strains the blood pressure is maintained by higher peripheral vascular resistance which at first is due to neurogenic vasoconstriction. Membrane changes may be involved. Regional cerebral blood flow is reduced, especially in areas of the brain fed by recurrent branches. Body weight is lower than in SHR. Signs of stroke include piloerection, hyperkinesis, hyperirritability, aggressiveness and motion disturbance. 634612