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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the rat, the results of genetic linkage studies by "candidate" gene or "positional mapping" approaches have suggested that DNA sequences that regulate blood pressure may be located in the vicinity of the kallikrein gene family on chromosome 1, the gene for angiotensin-converting enzyme on chromosome 10, the renin gene on chromosome 13, and the major histocompatibility complex on chromosome 20. Some studies have also suggested that blood pressure regulatory genes may be located on the sex chromosomes. Pending the results of confirmatory studies, these experiments should be interpreted with caution. However, with confirmation of these studies, it should be possible to create a variety of new animal models that will provide excellent opportunities for investigating the molecular, biochemical, and physiologic determinants of high blood pressure. In addition, in genetic studies in humans with essential hypertension, it may be worthwhile to target chromosome regions that are homologous to those implicated in linkage studies of hypertension in rodents. By narrowing the focus on selected areas of the genome, experimental linkage studies in the rat may also be used to guide the detailed molecular approaches ultimately required to identify the specific DNA sequence alterations that give rise to increased blood pressure.
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PMID:Gene mapping in experimental hypertension. 132 57

1. Abnormal heat stress gene hsp70 expression has been demonstrated in organs as well as in cultured cells from spontaneously hypertensive rats and mice. 2. The polymorphism of hsp70, which is localized in the major histocompatibility complex, appears to segregate with a significant portion of hypertension. 3. Abnormal hsp70 expression may lead to anomalies in its feedback regulation, particularly since the steady state level of heat stress protein HSP70 seems to be lower in hypertensive than in normal animals. 4. Another biological consequence could be a modification of the effectiveness of cortisol, which may be involved in metabolic components of the pathogenesis of hypertension.
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PMID:Abnormal hsp70 gene expression: its potential key role in metabolic defects in hypertension. 144 10

Essential hypertension is a complex clinical disorder in which multiple environmental and genetic factors interact to increase blood pressure. To search for chromosome regions that contain genes regulating blood pressure, some investigators have begun to conduct linkage studies in rodent models of spontaneous hypertension. Preliminary results suggest that in the rat, blood pressure regulatory genes may be located in the vicinity of the kallikrein gene family on chromosome 1, the gene for angiotensin converting enzyme on chromosome 10, the renin gene on chromosome 13, and the major histocompatibility complex on chromosome 20. Some studies have also suggested that blood pressure regulatory loci may be located on the sex chromosomes. Although comparisons between humans and animals should be made with caution, it is hoped that the identification of genes regulating blood pressure in the rat might shed light on the pathogenesis of hypertension in humans.
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PMID:Genetic approaches to hypertension. 161 May 44

The involvement of an auto-immune mechanism has been suggested in the development and/or the maintenance of hypertension in male, genetically hypertensive rats of the Lyon strain (LH). The aim of this study was to determine whether hypertension may be transferred, by lymphoid cells, from hypertensive donors to male, normotensive rats of the Lyon strain (LN). Experiments designed to induce a resistance to hypertension in LH rats by transfer of lymphoid cells from LN animals were also performed. Since LH and LN are mismatched at the major histocompatibility complex, transfers of fetal liver cells (FLC) from fetuses of 13-14 days gestation were performed. These experiments demonstrate the ability of FLC to allow a prolonged survival (over 17 weeks) without graft versus host disease in the rat. As regards the blood pressure level, no LN recipient having received FLC from LH donor became hypertensive, thus showing that hypertension cannot be transferred by lymphoid cells in normotensive animals. Resistance to hypertension was so weakly transferred to hypertensive rats (results being significantly different only at 10 weeks post-grafting) that it may be considered doubtful.
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PMID:Fetal liver cell transplantation fails to transfer hypertension from genetically hypertensive rats to normotensive rats of the Lyon strain. 184 65

Genetically hypertensive animals such as spontaneously hypertensive rats (SHR) and mice are more sensitive to thermal stress than normotensive controls. Genetic breeding experiments have demonstrated that the gene responsible for thermosensitivity segregates with an increase in blood pressure in the F2 generation and represents a genetic locus of hypertension. Due to a higher transcription rate of the heat shock protein 70 (hsp70) gene, which is a major heat stress gene, the accumulation of hsp messenger (m)RNA is increased in hypertension. Higher thermosensitivity and increased hsp mRNA accumulation are also observed in neonatal cardiomyocytes and cultured vascular smooth muscle cells from SHR, suggesting that these abnormalities are primary in character. This higher hsp70 transcription rate in hypertension could be due to an abnormality in the promoter region, to an interaction between heat stress trans-acting factor and heat stress element within the promoter of hsp70 or to an abnormal activation of heat stress trans-acting factor. A study using recombinant inbred animals has indicated that RT1 complex gene(s), a major histocompatibility complex in the rat, may be involved in the development of hypertension. These findings, together with the fact that hsp70 is located in the major histocompatibility complex, suggest that hsp70 gene or associated genes within the RT1 complex are responsible for environmental control of the expression of hypertension.
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PMID:Heat stress genes in hypertension. 209 96

Five multigenerational kindreds with familial hypertension were typed for human leukocyte antigen (HLA) and blood group antigens to investigate genetic factors that influence variability in blood pressure. Pedigree analysis revealed that children of matings in which both parents were hypertensive had a significantly greater risk of hypertension than children of matings in which one parent or neither parent was hypertensive. Blood types N and MN were abnormally distributed among hypertensive as compared with normotensive members of white but not black families. The distribution of ABO and Rh types was not significantly different between hypertensive and normotensive siblings. When all possible pairings of siblings were examined for HLA haplotype sharing, abnormal distributions were observed among hypertensive sib pairs whereas the expected mendelian segregation was observed among hypertensive-normotensive sib pairs and normotensive-normotensive sib pairs. These results suggest the genetic factors controlling variation in blood pressure may include loci in the region of the MN locus on chromosome 4 and, possibly, the major histocompatibility complex on chromosome 6.
Hypertension 1987 Jun
PMID:Possible association of MN locus haplotypes with essential hypertension. 358 3

1. The HXB/BXH recombinant inbred (RI) strains, derived from the spontaneously hypertensive rat (SHR) and the normotensive Brown Norway (BN.1x) rat, represent a very useful system for gene mapping and for genetic analysis of certain model diseases, such as spontaneous hypertension. 2. These RI strains were genotyped in multiple genetic polymorphisms and characterized in blood pressure and some intermediate phenotypes. 3. The analysis of RI strains has revealed that (i) a gene in the vicinity of the major histocompatibility complex (RT1) on chromosome 20, a kallikrein-related gene on chromosome 4 and the renin gene on chromosome 13 were significantly associated with blood pressure, and (ii) Na+ leak in red blood cells correlated with blood pressure whereas relative heart and kidney weights as well as platelet aggregation did not.
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PMID:Use of recombinant inbred strains for evaluation of intermediate phenotypes in spontaneous hypertension. 788 82

Thermosensitivity has been demonstrated in hypertensive rats and mice, and hypertension is frequent in hyperthermia-susceptible pigs. We have demonstrated that thermosensitivity segregates with hypertension in mice as a recessive trait in a single locus termed Tms. Since thermosensitivity can be demonstrated in cells obtained from neonatal hypertensive animals and persists after several passages in culture, it was of interest to study its cellular determinants. We undertook studies of candidate genes of cellular thermosensitivity, hsp70 being the major heat stress gene. First, we have observed an enhanced hsp70 mRNA accumulation in the hypertensive rat, mouse and human after heat shock of the whole animal, of its isolated organs or cultured cells. This increased accumulation of hsp70 mRNA in hypertension is due to its increased transcriptional rate. A restriction fragment length polymorphism (RFLP) of hsp70 was documented in hypertensive rats, which allowed the study of the segregation of this locus with hypertension in recombinant inbred strains of rats. At least one copy of hsp70 has been localized in RT1, the major histocompatibility complex of the rat, with polymorphism demonstrated with BamHI outside of the coding region of hsp70. This polymorphism segregates with 15 mmHg of systolic blood pressure. More recently, our studies led us to identify a polymorphism in another heat stress gene, hsp27. This polymorphism has been identified by PCR SSCP and is located in the 3' region, close to the termination translation codon.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The stress gene in hypertension]. 790 84

Dietary sodium intake has long been considered an important factor in the genesis and maintenance of hypertension in both humans and experimental animals. To identify the possible association between salt sensitivity and genes of the major histocompatibility complex (RT1 complex), we studied the blood pressure response to an 8% NaCl diet in normotensive Lewis rats, spontaneously hypertensive rats (SHR), and Lewis.1K congenic rats (congenic to Lewis with the SHR main histocompatibility complex RT1). During the first 4 weeks of a high salt diet, the blood pressure increase was the same in SHR and Lewis.1K congenic rats. Thus, the presence of a small segment of SHR chromosome 20 with genes of the RT1 complex (and closely related genes) in the Lewis genome sensitized the blood pressure of these animals to the hypertensive effects of a high salt diet. Genes of the RT1 complex influenced the salt-induced increase of relative kidney weight more than that of relative heart weight. Our results support the hypothesis that some alleles within or close to the RT1 complex might be responsible for the higher sensitivity of hypertensive individuals to certain environmental stressors, including high salt intake.
Hypertension 1994 Dec
PMID:Association of salt sensitivity in rats with genes of the major histocompatibility complex. 799 20

It was recognized that recombinant inbred strains are a very powerful system for the study of the genetics of hypertension, linkage analysis and gene mapping. Such set of recombinant inbred strains has been developed in the cooperation of Prof V. Kren and Dr. M. Pravenec in Prague. These recombinant inbred strains were used to search for the genes of spontaneous hypertension and to test the phenotypic differences. It was found that 1) the major histocompatibility complex of the rats showed a significant association with blood pressure, 2) the restriction fragment length polymorphism in kallikrein gene family as well as renin gene cosegregated with blood pressure, 3) Na+ leak in red blood cells cosegregated with blood pressure, 4) the relative heart and kidney weights are not closely related to mean arterial pressure and 5) the platelet aggregation and blood pressure are independent traits. The results indicate the usefulness of recombinant inbred strains in the analysis of the relationship between phenotype and genotype.
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PMID:Recombinant inbred strains in hypertension research. 799 91


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