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dc.contributor.author | Chamorro-Jorganes, Aranzazu | |
dc.contributor.author | Grande, Maria Teresa | |
dc.contributor.author | Herranz, Beatriz | |
dc.contributor.author | Jerkic, Mirjana | |
dc.contributor.author | Griera, Mercedes | |
dc.contributor.author | González Núñez, María | |
dc.contributor.author | Santos de Dios, Eugenio Miguel | |
dc.contributor.author | Rodríguez-Puyol, Diego | |
dc.contributor.author | López-Novoa, José Miguel | |
dc.contributor.author | Rodriguez-Puyol, Manuel | |
dc.date.accessioned | 2024-02-05T12:16:03Z | |
dc.date.available | 2024-02-05T12:16:03Z | |
dc.date.issued | 2010-09 | |
dc.identifier.citation | Chamorro-Jorganes, A., Grande, M. T., Herranz, B., Jerkic, M., Griera, M., Gonzalez-Nuñez, M., Santos, E., Rodriguez-Puyol, D., Lopez-Novoa, J. M., & Rodriguez-Puyol, M. (2010). Targeted genomic disruption of h-ras induces hypotension through a NO-cGMP-PKG pathway-dependent mechanism. Hypertension (Dallas, Tex.: 1979), 56(3), 484-489. https://doi.org/10.1161/HYPERTENSIONAHA.110.152587 | es_ES |
dc.identifier.issn | 0194-911X | |
dc.identifier.uri | http://hdl.handle.net/10366/155341 | |
dc.description.abstract | [EN]The aim of the present experiments was to evaluate the differences in arterial pressure between H-Ras lacking mice and control mice and to analyze the mechanisms involved in the genesis of the differences. H-Ras lacking mice and mouse embryonic fibroblasts from these animals were used. Blood pressure was measured using 3 different methods: direct intraarterial measurement in anesthetized animals, tail-cuff sphygmomanometer, and radiotelemetry. H-Ras lacking mice showed lower blood pressure than control animals. Moreover, the aorta protein content of endothelial nitric oxide synthase, soluble guanylyl cyclase, and cyclic guanosine monophosphate-dependent protein kinase was higher in H-Ras knockout mice than in control animals. The activity of these enzymes was increased, because urinary nitrite excretion, sodium nitroprusside-stimulated vascular cyclic guanosine monophosphate synthesis, and phosphorylated vasoactive-stimulated phosphoprotein in aortic tissue increased in these animals. Furthermore, mouse embryonic fibroblasts from H-Ras lacking mice showed higher cyclic guanosine monophosphate-dependent protein kinase promoter activity than control cells. These results strongly support the upregulation of the nitric oxide-cyclic guanosine monophosphate pathway in H-Ras-deficient mice. Moreover, they suggest that H-Ras pathway could be considered as a therapeutic target for hypertension treatment. | es_ES |
dc.description.sponsorship | Ministerio de Educación y Ciencia; Ministerio de Sanidad; Junta de Castilla León | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Lippincott Williams & Wilkins | es_ES |
dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.subject | Arterial pressure | es_ES |
dc.subject | cGMP-dependent protein kinase | es_ES |
dc.subject | Cyclic GMP | es_ES |
dc.subject | H-Ras protein | es_ES |
dc.subject | Nitric oxide | es_ES |
dc.subject | Soluble guanylyl cyclase | es_ES |
dc.subject.mesh | Aorta | * |
dc.subject.mesh | Fibroblasts | * |
dc.subject.mesh | Cells | * |
dc.subject.mesh | Nitric Oxide | * |
dc.subject.mesh | Statistics | * |
dc.subject.mesh | Blood Pressure | * |
dc.subject.mesh | Cyclic GMP | * |
dc.subject.mesh | Hypotension | * |
dc.subject.mesh | Cyclic GMP-Dependent Protein Kinases | * |
dc.subject.mesh | Guanylate Cyclase | * |
dc.subject.mesh | Phosphorylation | * |
dc.subject.mesh | Nitric Oxide Synthase Type III | * |
dc.subject.mesh | Immunohistochemistry | * |
dc.subject.mesh | Animals | * |
dc.subject.mesh | Signal Transduction | * |
dc.subject.mesh | Up-Regulation | * |
dc.subject.mesh | ras Proteins | * |
dc.subject.mesh | Mice | * |
dc.title | Targeted genomic disruption of h-ras induces hypotension through a NO-cGMP-PKG pathway-dependent mechanism | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.relation.publishversion | https://doi.org/10.1161/HYPERTENSIONAHA.110.152587 | es_ES |
dc.identifier.doi | 10.1161/HYPERTENSIONAHA.110.152587 | |
dc.relation.projectID | SAF2004-07845-C02 | es_ES |
dc.relation.projectID | SAF2004-07845-C02-01 | es_ES |
dc.relation.projectID | SAF2007-6389 | es_ES |
dc.relation.projectID | SAF 2007-623471 | es_ES |
dc.relation.projectID | PI070695 | es_ES |
dc.relation.projectID | RD6/0016 | es_ES |
dc.relation.projectID | SA001/C05 | es_ES |
dc.relation.projectID | SA029/A05 | es_ES |
dc.relation.projectID | GR100 | es_ES |
dc.rights.accessRights | info:eu-repo/semantics/embargoedAccess | es_ES |
dc.identifier.pmid | 20679183 | |
dc.identifier.essn | 1524-4563 | |
dc.journal.title | Hypertension (Dallas, Tex. : 1979) | es_ES |
dc.volume.number | 56 | es_ES |
dc.issue.number | 3 | es_ES |
dc.page.initial | 484 | es_ES |
dc.page.final | 489 | es_ES |
dc.type.hasVersion | info:eu-repo/semantics/acceptedVersion | es_ES |
dc.subject.decs | inmunohistoquímica | * |
dc.subject.decs | fibroblastos | * |
dc.subject.decs | hipotensión | * |
dc.subject.decs | transducción de señales | * |
dc.subject.decs | ratones | * |
dc.subject.decs | óxido nítrico | * |
dc.subject.decs | guanilato ciclasa | * |
dc.subject.decs | regulación positiva | * |
dc.subject.decs | proteínas ras | * |
dc.subject.decs | proteínas cinasas dependientes de GMP cíclico | * |
dc.subject.decs | presión sanguínea | * |
dc.subject.decs | aorta | * |
dc.subject.decs | células | * |
dc.subject.decs | animales | * |
dc.subject.decs | estadísticas | * |
dc.subject.decs | GMP cíclico | * |
dc.subject.decs | óxido nítrico sintasa de tipo III | * |
dc.subject.decs | fosforilación | * |
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GFCYR. Artículos [11]