Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 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

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

Spontaneously hypertensive rats (SHR) are one of the most common animal models used to study essential hypertension in humans. Because SHR and normotensive Wistar Kyoto (WKY) rats were both established from the same parental, normotensive Wistar stock, WKY animals have been used almost exclusively as control animals in studies of SHR. Recently, the suitability of WKY rats as normotensive controls for SHR has been challenged. To establish whether or not SHR and WKY rats share the same immunologic backgrounds, we initially performed a series of skin grafting experiments on these animals. In all cases, grafts of SHR donor skin to WKY recipients and of WKY donor skin to SHR recipients resulted in complete rejection within 7 to 10 days. In addition, grafts of WKY donor skin to other WKY recipients resulted in graft rejection. By contrast, skin grafts between SHRs were always accepted. To further characterize the genetic distinctions between SHR and WKY rats, allelic profiles based on a series of immunologic and biochemical markers were established for each strain. These findings clearly establish that SHR and WKY rats differ at the major histocompatibility complex, in specific blood group antigens, and in a panel of isozymic markers. Moreover, whereas SHRs have the same genetic profiles irrespective of source, some colonies of WKY rats are outbred, as judged by their variant allelic profiles.
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PMID:Spontaneously hypertensive and Wistar Kyoto rats are genetically disparate. 166 50

Six patients treated with captopril for severe essential hypertension were studied to determine whether the drug significantly altered circulating peripheral blood T (Thymus derived) lymphocytes and T lymphocyte subsets. OKT3+ (functionally mature T lymphocytes), OKT4+ (class II major histocompatibility complex [MHC] reactive T lymphocytes) and OKT8+ (class I MHC reactive T lymphocytes) T lymphocytes were monitored using monoclonal antibodies and flow cytometry before commencement of treatment and then at intervals during 14 months of captopril administration. Results showed a significant increase in the absolute numbers of OKT4+ cells at 2 h (p less than 0.05) and a decrease at 12 weeks (p less than 0.01) during captopril treatment. These findings indicate that captopril has an effect on cellular immunity in vivo.
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PMID:Effects of captopril on circulating T lymphocyte subsets. 330 81

The development of stress drives a host of biological responses that include the overproduction of a family of proteins named heat shock proteins (HSPs), because they were initially studied after heat exposure. HSPs are evolutionarily preserved proteins with a high degree of interspecies homology. HSPs are intracellular proteins that also have extracellular expression. The primary role of HSPs is to protect cell function by preventing irreversible protein damage and facilitating molecular traffic through intracellular pathways. However, in addition to their chaperone role, HSPs are immunodominant molecules that stimulate natural as well as disease-related immune reactivity. The latter may be a consequence of molecular mimicry, generating cross-reactivity between human HSPs and the HSPs of infectious agents. Autoimmune reactivity driven by HSPs could also be the result of enhancement of the immune response to peptides generated during cellular injury and of their role in the delivery of peptides to the major histocompatibility complex in antigen-presenting cells. In humans, HSPs have been found to participate in the pathogenesis of a large number of diseases. This review is focused on the role of HSPs in atherosclerosis and essential hypertension.
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PMID:Heat shock proteins and cardiovascular disease. 2960 92

Autoimmunity is increasingly recognized as having a central role in essential hypertension. Heat shock proteins (HSPs) are immunodominant molecules with high interspecies homology and autoimmune reactivity directed against HSP70 may play a role in the pathogenesis of hypertension. Autoimmunity to HSP70 may result from molecular mimicry between human HSP and bacterial HSP or, alternatively, as a response to HSP70-peptide complexes generated during cellular stress and delivered to the major histocompatibility complex by antigen-presenting cells. HSP70 is increased in the circulation and kidney of hypertensive patients, and genetic polymorphisms of HSP70 are associated with essential hypertension. Depending on the route and conditions of administration, HSP70 may induce or suppress immune-related inflammation. Renal inflammation induced by immunity to HSP70 causes hypertension in laboratory animals, and administration of specific peptide sequences of HSP70 results in a protective anti-inflammatory response that prevents and corrects salt-induced hypertension. Potential therapeutic uses of HSP70 in essential hypertension deserve to be investigated. LINKED ARTICLES: This article is part of a themed section on Immune Targets in Hypertension. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.12/issuetoc.
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PMID:The role of autoimmune reactivity induced by heat shock protein 70 in the pathogenesis of essential hypertension. 2967 84