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Strain: FHH

Symbol: FHH
Strain: FHH
Full Name: Fawn Hooded Hypertensive
RGD ID: 60993
RRID: RGD_60993
Ontology ID: RS:0000017
Also known as: FHR; RGD:68039; RS:0000346
Type: inbred
Source: University of Colorado Health Science Center, Denver, Colorado
Origin: An outbred stock of fawn hooded rats introduced into Europe by Tschopp in the early 1970s. Maintained as an outbred stock until the mid-1980s, then brother x sister mating initiated by A.P. Provoost to produce two strains designated FHH (also known as FHR) and FHL, which differ in hypertension and proteinuria. The colony was transferred to Erasmus University.
Genetic Markers: a,h,r.
Coat Color: Fawn Hooded.
Inbred Generations: F16 (Brown et al,1996).
Last Known Status: Unknown





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References


Region

Strain QTL Data
Symbol Name Trait
Bp197 Blood pressure QTL 197 arterial blood pressure trait   (VT:2000000)    
BpQTLcluster14 Blood pressure QTL cluster 14 arterial blood pressure trait   (VT:2000000)    
Rf2 Renal disease susceptibility QTL 2 urine protein amount   (VT:0005160)    

Additional Information

RGD Curation Notes
Note Type Note Reference
strain_life_disease Developes focal and segmental glomerular sclerosis, systemic hypertension and proteinuria at ayoung age, but these effects are more marked in FHH than FHL (Simons et al, 1993). The renal disease and hypertension are under independent genetic control, and both appear to be independent of the red-eyed dilution gene which causes platelet storage disease (Brown et al,1996). Glomerular filtration rate (GFR), renal blood flow (RBF), and glomerular capillary pressure (PGC) are elevated in FHH rats suggest that the control of renal vascular resistance may be altered in this strain. 1004
strain_life_disease Developes focal and segmental glomerular sclerosis, systemic hypertension and proteinuria at ayoung age, but these effects are more marked in FHH than FHL (Simons et al, 1993). The renal disease and hypertension are under independent genetic control, and both appear to be independent of the red-eyed dilution gene which causes platelet storage disease (Brown et al,1996). Glomerular filtration rate (GFR), renal blood flow (RBF), and glomerular capillary pressure (PGC) are elevated in FHH rats suggest that the control of renal vascular resistance may be altered in this strain. 61090
strain_life_disease Developes focal and segmental glomerular sclerosis, systemic hypertension and proteinuria at ayoung age, but these effects are more marked in FHH than FHL (Simons et al, 1993). The renal disease and hypertension are under independent genetic control, and both appear to be independent of the red-eyed dilution gene which causes platelet storage disease (Brown et al,1996). Glomerular filtration rate (GFR), renal blood flow (RBF), and glomerular capillary pressure (PGC) are elevated in FHH rats suggest that the control of renal vascular resistance may be altered in this strain. 634612
strain_life_disease A good model for platelet storage pool deficiency with low blood serotinin level than the BN rats. The blood coagulation time and platelet count is normal. 1300411
strain_other Have Rab38 Met1Ile mutation which is responsible for fawn-hooded pigmentary dilution and platelet storage pool deficiency 1300411
strain_phys_biochem Autoregulation of renal blood flow (RBF) is impaired in FHH rats before the development of glomerulosclerosis and suggest that an abnormality in the control of renal vascular resistance may contribute to the development of proteinuria and renal failure in this strain of rats. RBF and Glomerular filtration rate (GFR) are markedly elevated in FHH rats compared with values observed in fawn-hooded low blood pressure (FHL) rats. Urinary protein excretion was directly dependent on the changes in renal perfusion pressure (RPP) in FHH rats. The mechanism involved in this unusual pressure proteinuric response may be dependent on the GFR and the impaired autoregulation of RBF and GFR in response to elevations in RPP. 1004
strain_phys_biochem Autoregulation of renal blood flow (RBF) is impaired in FHH rats before the development of glomerulosclerosis and suggest that an abnormality in the control of renal vascular resistance may contribute to the development of proteinuria and renal failure in this strain of rats. RBF and Glomerular filtration rate (GFR) are markedly elevated in FHH rats compared with values observed in fawn-hooded low blood pressure (FHL) rats. Urinary protein excretion was directly dependent on the changes in renal perfusion pressure (RPP) in FHH rats. The mechanism involved in this unusual pressure proteinuric response may be dependent on the GFR and the impaired autoregulation of RBF and GFR in response to elevations in RPP. 61090
strain_phys_biochem Autoregulation of renal blood flow (RBF) is impaired in FHH rats before the development of glomerulosclerosis and suggest that an abnormality in the control of renal vascular resistance may contribute to the development of proteinuria and renal failure in this strain of rats. RBF and Glomerular filtration rate (GFR) are markedly elevated in FHH rats compared with values observed in fawn-hooded low blood pressure (FHL) rats. Urinary protein excretion was directly dependent on the changes in renal perfusion pressure (RPP) in FHH rats. The mechanism involved in this unusual pressure proteinuric response may be dependent on the GFR and the impaired autoregulation of RBF and GFR in response to elevations in RPP. 634612