Strain information
 NBRP Rat No: 0880  Strain name: GH/Htru  Commmon Name: GH, genetically hypertensive rat Rat Genome Database
Principal Investigator:  Scott Rhodes  University of Otago       University of Otago,HTRU office,Room 322 Hercus Building,58 Hanovar Street,Dunedin     Otago     New Zealand
Tel: +6434797187    Fax: N/A Email: scott.rhodes@otago.ac.nz
Preservation Status:   Embryo        Sperm       Living Animals
Coat Color  white (albino)
Inbred Generations  Inbr.F31+?
Usage Restrictions  The following terms and conditions will be requested by the DEPOSITOR.
In publishing the research resoults to be obtained by use of the BIOLOGICAL RESOURCE, an acknowlodgment to the DEPOSITOR is requested.
Genetic Status
 Inbred  Segregating  Congenic  Consomic  Recombinant
 Coisogenic  Spont. Mutant  Transgene  Ind. Mutant  Category Other 
Comercial Availability
Research Category
 Diabetes Obesity  Neurobiology  Ophthalmology  Dentistry  Cardio Hypertension
 Cancer  Metabolism  Otorhinology  Immunology  Infectious
 Osteosis  Internal Organ  Dermatology  Reproduction  Development
 Behavior  Hematology  Urology  Pharmacology  Research Area Others 
 Control Strain  Marker Strain
Gene Affected The causative gene of GH rat has not yet been identified.
Origin 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). 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 about two-fold that or normal rats, and substance P containing sensory neurone numbers are also elevated (Bakhle and Bell, 1994).
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 about two-fold that or normal rats, and substance P containing sensory neurone numbers are also elevated (Bakhle and Bell, 1994).
Breeding Conditions Maintained in homozygous condition. Fair Breeding performance, No Special Diets or Drinking Water Good Mothers, non aggressive.
Genotyping no genotyping necessary
References Bakhle Y. S. and Bell C. (1994) Increased numbers of substance P-containing sensory neurons in a rat strain with a genetic neurotrophic defect. Neuropeptides 27, 169-174. \par Hendry I. A. and Bell C. (1993) Age-related-changes in tyrosine-hydroxylase and choline- acetyltransferase in sympathetic-ganglia of a rat strain with reduced sympathetic neuron numbers. Journal of Neurochemistry 60, 1093-1097. \par Heslop B. F. and Phelan E. L. (1973) The GH and AS hypertensive rat strains. Lab. Anim. 7, 41-46. \par Ledingham J. M. and Millar J. A. (1993) Stereological studies on mesenteric resistance artery structure in New-Zealand Genetically Hypertensive and control rats. Clin. Exp. Pharmacol. Physiol. 20, 359-361. \par Phelan E. L. (1968) The New Zealand strain of rats with genetic hypertension. N.Z. Med. J. 67, 334-344. \par Simpson F. O., Phelan E. L., Clark D. W. J., Jones D. R., Gresson C. R., Lee D. R., and Bird D. L. (1973) Studies on the New Zealand strain of genetically hypertensive rats. Clin. Sci. Molec. Med. 45, 15s-21s. \par Simpson F. O. and Phelan E. L. (1984) Hypertension in the Genetically Hypertensive strain, in Handbook of Hypertension Vol. 4. Experimental and genetic models of hypertension (de Jong W., ed), pp. 200-223. Elsevier, Amsterdam, New York, Oxford. \par Simpson F. O., Phelan E. L., Ledingham J. M., and Millar J. A. (1994) Hypertension in the Genetically Hypertensive (GH) strain, in Handbook of Hypertension Vol. 16 Experimental and Genetic Models of Hypertension (Ganten D. and de Jong W., eds), pp. 228-271. Elsevier, Amsterdam, New York, Oxford. \par Smyth D. D., Phelan E. L., and Stanko C. (1992) Renal alpha-2-adrenoceptors in New-Zealand genetically hypertensive rats. Journal of Autonomic Pharmacology 12, 73-80. \par
Additional strain information