Genetic Control of Blood Pressure in Spontaneously Huypertensive Rats (SHR)

Tanase, Hisao

doi:10.1538/expanim1978.28.4_519

Cited by 26 publications

(14 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This has proven to be the case. Tanase 37 was able to transfer the SHR allele at this locus to Donryu inbred rats by repeated backcrossing and selection, that is, congeneic strains were developed for this locus. With these congeneic strains Tanase clearly demonstrated for blood pressure 1:1 bimodal distributions in backcross populations, and 1:2:1 trimodal distributions for blood pressure in F 2 populations.…”

Section: Discussionmentioning

confidence: 99%

A genetic locus (Hyp-2) controlling vascular smooth muscle response in spontaneously hypertensive rats.

Rapp¹

1982

Hypertension

View full text Add to dashboard Cite

SUMMARY Aortic vascular smooth muscle from spontaneously hypertensive rats (SHR) is known to respond in vitro to nonphysiologic cations with greater contraction than vascular smooth muscle from certain normotensive control stocks. The pattern of inheritance of the response of aortic rings to cobalt (Co 2+ ) in vitro was determined. The test characteristic utilized was the cobalt response ratio (CRR) defined as the contractile response to 0.6 ^M Co 2+ divided by the response given by maximal stimulation with 10 /xM Co 2 *. The SHR were crossed with Dahl salt-resistant rats that had been inbred for 21 generations (R/JR strain) to produce F,, F 2 , and backcross populations. The CRR was 0.90 ± 0.011 in SHR, 0.74 ± 0.016 in F,, and 0.38 ± 0.031 in R/JR. The F, value was significantly higher than the midparental value indicating partial SHR dominance. The F| males from reciprocal crosses had similar CRR indicating no sex-linked effect. In the backcross to the R/JR, the CRR showed a bimodal distribution segregating one intermediate type: one R/JR type. In the backcross to the SHR the CRR showed a unimodal distribution. In F 2 rats there was a bimodal distribution segregating three intermediate type: one R/JR type. In F 2 rats there was a significant (p < 0.005) blood pressure difference of 9.7 mm Hg between phenotypes. It is concluded that there is an autosomal locus (named "Hyp-2" for hypertension locus number 2) controlling vascular smooth muscle response to Co 2+ , which exhibits partially dominant inheritance. Some attention has been paid to determining whether the vascular smooth muscle changes noted above are secondary results of hypertension or primary causes of hypertension. Four approaches have been tried and all indicated *hat the changes studied were primary. 1) Visceral 14 and vas deferens 15 smooth muscle as well as vascular smooth muscle showed abnormalities in SHR indicating that smooth muscle alterations in SHR were generalized and not restricted to vessel walls exposed to high blood pressure. 2) Smooth muscle from vascular beds in the leg when protected from hypertension by a proximal ligature showed similar properties to smooth muscle exposed to hypertension in SHR. 3) Following pharmacologic control of blood pressure in SHR from weaning, the vascular smooth muscle of SHR still showed its characteristic abnormalities.

show abstract

Section: Discussionmentioning

confidence: 99%

A genetic locus (Hyp-2) controlling vascular smooth muscle response in spontaneously hypertensive rats.

Rapp¹

1982

Hypertension

View full text Add to dashboard Cite

show abstract

“…14 - 16 However, these previous studies only indicated the possible relation of the autosomal loci to each other and not the interaction of the autosomal and Y chromosome components.…”

Section: Relation Of Y and Autosomal Componentsmentioning

confidence: 99%

Separate sex-influenced and genetic components in spontaneously hypertensive rat hypertension.

1991

View full text Add to dashboard Cite

“…If, on the other hand, as does seem possible in SHR, VOL 10, No 1, JULY 1987 been performed twice with SHR. 1718 Tanase 17 successfully transferred the allele from SHR at a major locus influencing blood pressure to normotensive inbred Donryu rats, and in a separate experiment, the Donryu allele at this major locus was successfully transferred to SHR. The fate of these congenic strains since 1979 is obscure.…”

Section: Hypertensionmentioning

confidence: 99%

Use and misuse of control strains for genetically hypertensive rats.

Rapp¹

1987

Hypertension

View full text Add to dashboard Cite

T HE article by Kurtz and Morris1 in this issue of Hypertension raises important issues with regard to the use of genetically hypertensive rats. These issues are 1) the origins of various stocks, 2) the definition and maintenance of the integrity of various stocks of interest in hypertension research, and 3) the construction, appropriateness, and use of control strains for comparison with hypertensive strains. The article by Kurtz and Morris 1 traces the tortured origin of the Wistar-Kyoto (WKY) "strain" as a control for spontaneously hypertensive rats (SHR); clearly, the need for a control strain here was an afterthought and not all WKY are likely to be genetically identical. Their article illustrates the frustration of leaving unanswered the question of how to obtain genetic information from a hypertensive strain.The problems relating to control strains originate, in my view, from the unrealistic and inappropriate expectations imposed on a comparison of a hypertensive and control strain rather than from the undefined origins and possible genetic inappropriateness of controls. It is obvious from the literature on SHR that many investigators compare SHR and WKY for some biochemical or physiological trait (call it "trait X") and then conclude that the strain difference in trait X may be causally related to blood pressure differences. The problem is that, with this kind of information, the strain difference in trait X may be the result (rather than the cause) of strain differences in blood pressure, or strain differences in trait X may be due to genetic drift. Genetic drift is the chance selection and fixation of the contrasting genes controlling trait X in the two different strains. Strain differences arising from genetic drift have nothing to do with strain differences in blood pressure.If trait X differs between a hypertensive and a normotensive control strain the appropriate conclusion is simply that there are strain differences in trait X and there are strain differences in blood pressure. Why make such comparisons if this is all that can be concluded? Obviously, one has to determine if strain differences exist in a trait of interest as a first step in determining if there is any difference worthy of further study. If there is no strain difference in trait X, then there is no genetic diversity to study. To unravel the cause and effect relationship between trait X and blood pressure, however, one must be willing to do more than make strain comparisons.The meaning of strain-differences in trait X vis-a-vis strain differences in blood pressure can be found by determining if trait X and blood pressure are genetically separable or inseparable. That is, one tests in breeding experiments whether the association of trait X and blood pressure (i.e., a component of blood pressure) is retained in genetically segregating populations (i.e., populations in which genes can recombine at random). If the gene (or genes) controlling trait X is one of the genes influencing blood pressure, then it will remain associated with an i...

show abstract

Genetic Control of Blood Pressure in Spontaneously Huypertensive Rats (SHR)

Cited by 26 publications

References 31 publications

A genetic locus (Hyp-2) controlling vascular smooth muscle response in spontaneously hypertensive rats.

A genetic locus (Hyp-2) controlling vascular smooth muscle response in spontaneously hypertensive rats.

Separate sex-influenced and genetic components in spontaneously hypertensive rat hypertension.

Use and misuse of control strains for genetically hypertensive rats.

Contact Info

Product

Resources

About