GH

Inbr.F31+?.

Colour: Albino.

Genet: c.

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).

---

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.

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.

Heslop B. F. and Phelan E. L. (1973) The GH and AS hypertensive rat strains. Lab. Anim. 7, 41-46.

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.

Phelan E. L. (1968) The New Zealand strain of rats with genetic hypertension. N.Z. Med. J. 67, 334-344.

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.

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.

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.

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.

---

INBRED STRAINS OF RATS
Updated 9 Apr. 1998
Michael FW Festing
MRC Toxicology Unit, Hodgkin Building,
University of Leicester, UK