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Strain Registration

Strain: GH

Symbol: GH
Strain: GH
RGD ID: 60984
Citation ID: RRID:RGD_60984
Ontology ID: RS:0000318
Type: inbred
Available Source: Not Available
Description: University of Otago Medical School from rats of Wistar origin imported from England in 1930. Selection for high blood pressure started by Smirk in 1955. A number of sublines have been developed. Closely related to strain AS (Heslop and Phelan 1973).
Genetic Markers: c
Coat Color: Albino.
Inbred Generations: F31+?
Last Known Status: Unknown





Experimental Data Annotations    Click to see Annotation Detail View

Rat Strain
Object SymbolSpeciesTermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
GHRatGH  IEA 7241799 RGD 

Vertebrate Trait
Object SymbolSpeciesTermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
GHRatarterial blood pressure trait  EXP 68932 RGD 

Phenotype Values via Phenominer Click to see Annotation Detail View

Related Phenotype Data for Term "GH" (RS:0000318)

Rat Strains:
Clinical Measurements:
Experimental Conditions:
Measurement Methods:

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. Inbred Strains Festing, MFW, Inbred Strains, The Laboratory Rat, 1979, Baker HK, Lindsey JR, Weisbroth SH, 55-72, Academic Press
2. Update to previous Strain Data Festing, MFW, Personal Communication Update, Feb-2000
3. RGD Strain RSO annotation pipeline RGD Automated Pipelines
4. New target regions for human hypertension via comparative genomics. Stoll M, etal., Genome Res 2000 Apr;10(4):473-82.

Region

Strain QTL Data
Symbol Name Trait
BpQTLcluster7 Blood pressure QTL cluster 7 arterial blood pressure trait   (VT:2000000)    

Additional Information

RGD Curation Notes
Note Type Note Reference
strain_characteristics Develops hypertension, cardiac hypertrophy and vascular disease (Phelan 1968, Simpson and Phelan 1984, Simpson et al, 1994). Heart rate about 20% greater, lower body fat and heart weight about 50% greater than in normotensive strains. Genetic hypertension in GH (but not SHR) may be associated with a defect in renal prostaglandin catabolism (Armstronag et al 1976).Strain characteristics in relation to SHR reviewed by Simpson et al (1973) and also in de Jong(1984). Systolic blood pressure is significantly lowered by Cilazapril (Ledingham et al, 1993). A study of the structure of the mesenteric resistance arteries shows that the media volume is increased early in life, possibly due to hypertrophy of the smooth muscle cells or an increase in the amount of extracellular matrix, or both. However, since hypertension is present at an early age,these effects may not be the primary cause of hypertension (Ledingham and Miller, 1993). The renal alpha-2-adenoceptor densitiy is increased compared with the normotensive control at 12, but not at 4 weeks of age. However, this is due to a decrease in the control rather than an increase in GH rats (Smyth et al, 1992). A sub-population of sympathetic ganglionic neurones die during the perinatal period, but these die much later in life in Wistar rats (Hendry and Bell, 1993).Levels of substance P in superior cervical ganglion, spinal cord, iris and trachea are abou ttwo-fold that or normal rats, and substance P containing sensory neurone numbers are also elevated (Bakhle and Bell, 1994). 1004
strain_characteristics Develops hypertension, cardiac hypertrophy and vascular disease (Phelan 1968, Simpson and Phelan 1984, Simpson et al, 1994). Heart rate about 20% greater, lower body fat and heart weight about 50% greater than in normotensive strains. Genetic hypertension in GH (but not SHR) may be associated with a defect in renal prostaglandin catabolism (Armstronag et al 1976).Strain characteristics in relation to SHR reviewed by Simpson et al (1973) and also in de Jong(1984). Systolic blood pressure is significantly lowered by Cilazapril (Ledingham et al, 1993). A study of the structure of the mesenteric resistance arteries shows that the media volume is increased early in life, possibly due to hypertrophy of the smooth muscle cells or an increase in the amount of extracellular matrix, or both. However, since hypertension is present at an early age,these effects may not be the primary cause of hypertension (Ledingham and Miller, 1993). The renal alpha-2-adenoceptor densitiy is increased compared with the normotensive control at 12, but not at 4 weeks of age. However, this is due to a decrease in the control rather than an increase in GH rats (Smyth et al, 1992). A sub-population of sympathetic ganglionic neurones die during the perinatal period, but these die much later in life in Wistar rats (Hendry and Bell, 1993).Levels of substance P in superior cervical ganglion, spinal cord, iris and trachea are abou ttwo-fold that or normal rats, and substance P containing sensory neurone numbers are also elevated (Bakhle and Bell, 1994). 634612