Restriction fragment length polymorphisms mapped in spontaneously hypertensive rats using kallikrein probes

Woodley-Miller, C; Chao, Julie; Chao, Lee

doi:10.1097/00004872-198911000-00003

Cited by 54 publications

(13 citation statements)

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“…Reduced urinary kallikrein excretion has also been described in a number of genetically hypertensive rats (10)(11)(12)(13). In addition, rat tissue kallikrein has been linked with blood pressure regulation by restriction fragment length polymorphism and cosegregation studies in genetically hypertensive rats ( 14,15 ). These findings suggest that low renal kallikrein levels may contribute to hypertension and high urinary kallikrein could have a protective effect against hypertension.…”

Section: Introductionmentioning

confidence: 88%

Direct gene delivery of human tissue kallikrein reduces blood pressure in spontaneously hypertensive rats.

Wang¹,

Chao²,

Chao³

1995

J. Clin. Invest.

135

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Hypertension is a multigene and multifactorial disorder affecting -25% of the population. To demonstrate potential therapeutic effects of human tissue kallikrein in hypertension, spontaneously hypertensive rats were subjected to somatic gene therapy. Two human tissue kallikrein DNA constructs, one under the promoter control of the metallothionein metal response element and the other under the control of the Rous sarcoma virus 3'-LTR, were generated. We delivered naked DNA constructs into spontaneously hypertensive rats via intravenous injection. The expression of human tissue kallikrein in rats was identified in the heart, lung, and kidney by reverse transcription polymerase chain reaction followed by Southern blot analysis and an ELISA specific for human tissue kallikrein. A single injection of both human kallikrein plasmid DNA constructs caused a sustained reduction of blood pressure which began 1 wk after injection and continued for 6 wk. A maximal effect of blood pressure reduction of 46 mmHg in rats was observed 2-3 wk after injection with kallikrein DNA as compared to rats with vector DNA (n = 6, P < 0.05).

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Section: Introductionmentioning

confidence: 88%

Direct gene delivery of human tissue kallikrein reduces blood pressure in spontaneously hypertensive rats.

Wang¹,

Chao²,

Chao³

1995

J. Clin. Invest.

135

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“…6 In fact, the blood pressure of hypertensive patients can be lowered temporarily by oral administration of pig pancreatic kallikrein. 78 Tissue kallikrein has been linked with blood pressure regulation by restriction fragment length polymorphisms 9 and the cosegregation of high blood pressure with a restriction fragment length polymorphism marking the kallikrein gene family in a hypertensive rat model. 10 Reduced urinary kallikrein excretion also has been described in a number of genetic hypertensive rats.…”

Section: Human Tissue Kallikrein Induces Hypotension In Transgenic Micementioning

confidence: 99%

Human tissue kallikrein induces hypotension in transgenic mice.

et al. 1994

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We investigated the role of the kallikrein-kinin system in blood pressure control by developing transgenic mice overexpressing human tissue kallikrein. Two lines of transgenic mice carrying the human tissue kallikrein gene under the control of the mouse metallothionein metal-responsive promoter were established. Human tissue kallikrein was identified in pancreas, salivary gland, kidney, liver, and spleen of the transgenic mice by a specific radioimmunoassay for human tissue kallikrein. The immunoreactive human tissue kallikrein reached high levels in the circulation. The linear displacement curves for the transgenic product were parallel with the human tissue kallikrein standard curve, indicating their immunologic identity. The expression of human tissue kallikrein transcript in the transgenic mice was further confirmed by Northern blot analysis and by reverse transcription-polymerase chain reaction followed by Southern blot. Both lines of transgenic mice had significantly lowered blood pressure (86.4±13.5 mm Hg [mean±SD], n=8 and 78.9±12.4 mm Hg, n=8) compared with control mice (10O.9±5.0 mm Hg, n=8). Induction with zinc did not lower the blood pressure further despite elevated expression of the transgene. Administration of aprotinin, a potent tissue kallikrein inhibitor, restored the blood pressure of the transgenic mice but had no significant effect on control littermates. Our findings raise the possibility of tissue kallikrein being a powerful modulator of blood pressure and provide a new animal model for the study of blood pressure regulation. (Hypertension. 1994^3:236-243.)-

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“…3 -5 In recent years, the analysis of genomic DNA using restriction fragment length polymorphisms (RFLPs) has been applied to studies of SHR. 6 - 12 Several reports have pointed out that the Wistar-Kyoto (WKY) rat from different sources showed substantial variance in DNA fingerprints, indicating that the WKY rat was genetically heterogeneous. 6 -7 By contrast, they showed that SHR from the different sources had the same DNA fingerprinting pattern, suggesting that SHR was a homogeneous inbred strain.…”

Section: T He Spontaneously Hypertensive Rat (Shr) Andmentioning

confidence: 99%

Genetic heterogeneity of the spontaneously hypertensive rat.

et al. 1991

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We examined DNA fingerprints of the spontaneously hypertensive rat from Shimane Institute of Health Science, Izumo, Japan, including seven substrains that were separated in the early stages of the establishment of the stroke-prone spontaneously hypertensive rat, and compared their fingerprints with those of rats from other sources. Obtained DNA fingerprints revealed that, in both the stroke-resistant spontaneously hypertensive rat and the Wistar-Kyoto rat, there is a substantial genetic difference between the rats from the National Institutes of Health and from Shimane Institute of Health Science. By contrast, only a small genetic difference was observed either between the rats from the National Institutes of Health and Charles River Laboratories or among the substrains of the spontaneously hypertensive rat in the Shimane Institute of Health Science. Further, in the strains from the Shimane Institute of Health Science, there were fingerprinting bands that could distinguish either the Wistar-Kyoto rat from all the substrains of the spontaneously hypertensive rat or the stroke-prone from the stroke-resistant spontaneously hypertensive rat in spite of their close genetic backgrounds. From the observations above, we concluded 1) that there is substantial genetic variance of the spontaneously hypertensive rat between the two major sources in the world, the National Institutes of Health and the Shimane Institute of Health Science and 2) that by DNA fingerprinting analysis, it is possible to identify the restriction fragment length polymorphisms that are specific for the spontaneously hypertensive rat or the stroke-prone spontaneously hypertensive rat These polymorphisms can be applied in the segregation study of the

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Restriction fragment length polymorphisms mapped in spontaneously hypertensive rats using kallikrein probes

Cited by 54 publications

References 0 publications

Direct gene delivery of human tissue kallikrein reduces blood pressure in spontaneously hypertensive rats.

Direct gene delivery of human tissue kallikrein reduces blood pressure in spontaneously hypertensive rats.

Human tissue kallikrein induces hypotension in transgenic mice.

Genetic heterogeneity of the spontaneously hypertensive rat.

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