Biometric genetic analysis of blood pressure in the spontaneously hypertensive rat.

Kurtz, Theodore W.; Casto, R. Michael; Simonet, Lizette; Printz, Morton P.

doi:10.1161/01.hyp.16.6.718

Cited by 17 publications

(10 citation statements)

References 24 publications

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“…Average systolic blood pressure of F1 and FZ are apparently lower than median values of the systolic blood pressure of the parent SHR and WKY. These results are compatible with those reported by Kurtz et al (1990), concluding that SHR may have several dominant anti-hypertensinogenic alleles. It is also shown that systolic blood pressure can be a good genetic marker instead of mean blood pressure in these rats.…”

Section: Discussionsupporting

confidence: 92%

“…Traditionally, by classical crosses between SHR and WKY rat, many researchers tried genetic biometric assays to determine the molecular etiology of hyperteniion. However, their results are rather controversial, except that SHR may have one or more hypertensinogenic gene(s) ( Kurtz et al 1990). Possible reason for the controversies may be genetic heterogeneity of the experimental rats, because the researchers use various SHR and WKY colonies in their experiments.…”

Section: Discussionmentioning

confidence: 99%

“…hypertension by several research groups (Tanase et al 1970; Yen et al 1974; Judy et al 1979;Harrap 1986; Kurtz et al 1990). However, the results are rather controversial, probably due to lack of a technical skill in the measurement of blood pressure or possible genetic heterogeneity of these strains.…”

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confidence: 99%

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Substrain Comparison of Genetically Hypertensive Rats Using DNA Fingerprinting, and Genetic Analysis of Blood Pressure in the Inbred Rats.

Katsuya

Higaki

Miki

et al. 1991

Tohoku J. Exp. Med.

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Using DNA fingerprinting, genetic heterogeneity or homogeneity was studied between substrains of spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats maintained in Japan. Using human myoglobin minisatellite 33.15 as a probe, we did not detect any inter-or intrasubstrain genetic heterogeneities in HinfI digests of SHR or WKY rat DNA. However, analysis of Sau3AI digests of rat DNA using mouse C-6 gene as a probe revealed intra-substrain heterogeneity of 1-2 DNA bands in one of the WKY rat substrains. In the other substrains of SHR and WKY rats, there existed no intra-substrain heterogeneities, but several inter-substrain heterogeneities were observed in both SHR and WKY rats. In another experiment using the inbred substrains of SHR and WKY rats which have been confirmed as genetically homogeneous, we produced F1 and F2 rats, and biometrically analyzed their systolic blood pressure. The results suggested that there may be 1-4 dominant antihypertensinogenic genes with high heritability of 0.6-0.7.hypertension ; gene ; spontaneously hypertensive rat ; Wistar-Kyoto rat ; DNA fingerprinting Since the spontaneously hypertensive rat (SHR) has been developed by Okamoto and Aoki (1963), it has become a widely studied model of human essential hypertension. The SHR and its normotensive control of Wistar-Kyoto (WKY) rat were first introduced to National Institute of Health, USA, and then distributed to scientific farms world-wide. Many colonies of substrains of SHR or WKY rats are now maintained, but intra-colony or inter-colony variations should have been evolved among them (Yamori 1989). Classical mating experiments with SHR and WKY rats have been performed for the genetic analysis of

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

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Substrain Comparison of Genetically Hypertensive Rats Using DNA Fingerprinting, and Genetic Analysis of Blood Pressure in the Inbred Rats.

Katsuya

Higaki

Miki

et al. 1991

Tohoku J. Exp. Med.

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“…Counting of the radioactivity in these spots confirmed Marche's observation that more 32 P was incorporated into phosphatidylcholine in SHRSP, but the differences observed in the current study were less pronounced than the 10-to 16-fold difference reported previously. 31 The explanation for these discrepancies is not clear; the possibilities to consider are: 1) betweenstrain differences in genetically hypertensive rats obtained from commercial suppliers as compared with inbred colonies used in this study 50 and 2) time of exposure of the x-ray film to TLC plates; the total lipid-associated radioactivity per microgram of protein tends to be low in platelets and longer exposure (up to 48 hours) is needed to visualize the phosphatidylcholine in platelets from WKY.…”

Section: Jones and Hartmentioning

confidence: 97%

Lipid bilayer in genetic hypertension.

et al. 1991

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Membrane microviscosity, phospholipid composition, and turnover were measured in cultured vascular smooth muscle cells isolated from mesenteric arteries of stroke-prone spontaneously hypertensive and age-matched, normotensive Wistar-Kyoto rats. Membrane microviscosity, measured with fluorescence polarization, revealed greater microviscosity (lower fluidity) of the membranes isolated from smooth muscle cells from hypertensive as compared with those isolated from normotensive rats (p<0.01). Preincubation of membranes from hypertensive rats with 5 mM calcium reduced membrane microviscosity in "core" and in "surface" regions of the bilayer toward values observed in Wistar-Kyoto rats. Phospholipid composition did not differ between intact aortas and cultured mesenteric cells or between those tissues obtained from normotensive and from hypertensive rats. The total lipid-associated radioactivity was significantly lower in cells from stroke-prone spontaneously hypertensive rats than in those from Wistar-Kyoto controls (/?<0.01). Phosphatidylcholine incorporated 70% and phosphatidylinositol 16% of total lipid-associated radioactivity, with no difference between cells from hypertensive and normotensive animals. Turnover of phosphatidylethanolamine was greater in cells from Wistar-Kyoto rats (p=0.02), whereas turnover of phosphatidylserine was greater in cells from stroke-prone spontaneously hypertensive rats (p=0.04). The greater microviscosity of the lipid bilayer in hypertension is a generalized defect of the matrix in which the transport proteins function. We hypothesize that this defect is responsible for the multiple abnormalities of membrane transport systems that have been described in genetic hypertension. (Hypertension 1991;18:748-757)

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“…Environmental conditions for the tests were carefully controlled (same room, same tester, quiet environment, mild warming). The method was also validated by a biometric ANOVA of the blood pressure levels in Fj and F 2 populations as described by Kurtz et al 4 The percentage of the variance owing to genetic compared with environmental factors (including "noise" resulting from the method of estimation) was calculated as (variance in F 2 progeny-variance in F, progeny)-;-(variance in F 2 ). After 17 and 32 days on the high salt diet, the values were 79% and 88%, respectively, and compared favorably with the value of 60% in the study of Kurtz et al 4 …”

Section: Blood Pressure Estimationsmentioning

confidence: 99%

Inheritance of salt-dependent hypertension in the inbred Dahl rat.

Abbott

Schachter

1994

Hypertension

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The mode of inheritance of salt-dependent hypertension in the inbred Dahl salt-sensitive rat strain was examined by genetic crosses with the corresponding salt-resistant strain. The blood pressure responses to ingestion of a high Nad (8%) diet defined three phenotypes: early onset (within 17 days) of systolic hypertension, defined as greater than or equal to 140 mm Hg, the parental salt-sensitive phenotype; late onset of systolic hypertension requiring 50 to 60 days in males and more than 200 days in females, characteristic of the F, progeny; and normotension, less than 140 mm Hg, the parental salt-resistant phenotype. The frequencies of the phenotypes observed among 91 F 2 progeny and 45 progeny of the backcross to parental salt-sensitive animals agree well with values predicted by a model in which two autosomal, unlinked, allelic loci, termed a and p, determine the inheritance. For F 2 male progeny, the T he phenotypic characteristics of genetically determined, salt-dependent hypertension in the Dahl rat strain have been widely studied and well summarized in periodic reviews.1 ' 2 The mode of inheritance of the disorder, however, remains unclear. Knudsen et al 3 examined F,, F 2 , and backcross progeny in a prodigious study of approximately 2000 outbred, Brookhaven, salt-sensitive (S) and salt-resistant (R) rats over a 6-year period. Focusing on the systolic blood pressure levels observed after rats had been 24 weeks on an 8% NaCl diet, the authors noted a broad, apparently unimodal distribution of values and concluded that the inheritance was polygenic and complex. The simplest model to account for the distribution of the blood pressure levels assumed two unlinked, autosomal, allelic loci. In males, the S alleles were assumed to contribute additivery, so rats with 0 to 1, 2, or 3 to 4 such alleles should exhibit the salt-resistant, an intermediate, or the salt-sensitive blood pressure level, respectively. Females were postulated to be similar except for dominance of the R allele at one locus. While this study is an important contribution, it has a number of limitations. The mating of outbred, genetically inhomogeneous strains makes interpretation uncertain. Focus on the blood pressure levels at 24 weeks ignores the significance of earlier hypertensive responses and entails the complications of significant prior mortality and

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Biometric genetic analysis of blood pressure in the spontaneously hypertensive rat.

Cited by 17 publications

References 24 publications

Substrain Comparison of Genetically Hypertensive Rats Using DNA Fingerprinting, and Genetic Analysis of Blood Pressure in the Inbred Rats.

Substrain Comparison of Genetically Hypertensive Rats Using DNA Fingerprinting, and Genetic Analysis of Blood Pressure in the Inbred Rats.

Lipid bilayer in genetic hypertension.

Inheritance of salt-dependent hypertension in the inbred Dahl rat.

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