Publicación:
The role of the L-arginine-nitric oxide pathway in preeclampsia

dc.contributor.authorLopez-Jaramillo, Patriciospa
dc.contributor.authorArenas, William D.spa
dc.contributor.authorGarcía, Ronald G.spa
dc.contributor.authorRincón, Melvin Y.spa
dc.contributor.authorLópez Casillas, Marcosspa
dc.date.accessioned2019-08-29T16:56:05Zspa
dc.date.available2019-08-29T16:56:05Zspa
dc.date.issued2008-08-01spa
dc.description15 p.spa
dc.description.abstract: Preeclampsia (PE) is a major cause of maternal and perinatal mortality, especially in developing countries. Its etiology involves multiple factors, but no specific cause has been identified. Evidence suggests that clinical manifestations are caused by endothelial dysfunction. Nitric oxide (NO), which is synthesized from L-arginine in endothelial cells by the endothelial nitric oxide synthase (eNOS), provides a tonic dilator tone and regulates the adhesion of white blood cells and platelet aggregation. Alterations in the L-arginine-NO pathway have been associated with the development of PE. Various studies, reporting decreased, elevated or unchanged levels of nitrite (NO2) and nitrate (NO3), two end products of NO metabolism, have been published. Our group contributed to those contradictory reports describing cases of PE with both elevated and decreased levels of NO2 and NO3. Apparently, diminished levels of NO could be related to deficiencies in the ingestion of dietary calcium associated to low levels of plasma ionic calcium, which is crucial to the eNOS’ activity. Also, low levels of NO could be associated with the presence of eNOS polymorphisms or the presence of increased levels of ADMA, the endogenous inhibitor of NO. High levels of NO associated to low levels of cGMP suggest a decreased bioactivity of NO, which is probably related to an increased degradation of NO caused by a high production of superoxide in states of infection and inflammation. The present article analyses and reviews the reported paradoxical roles of the L-arginine-NO pathway in PE and gives a possible explanation for these results.spa
dc.format.mimetypeapplication/pdfspa
dc.identifier.doi10.1177/1753944708092277spa
dc.identifier.issn1753-9455spa
dc.identifier.issn1753-9447spa
dc.identifier.urihttps://repositorio.udes.edu.co/handle/001/3691spa
dc.language.isoengspa
dc.relation.ispartofTherapeutic Advances in Cardiovascular Diseaseeng
dc.relation.ispartofseriesTherapeutic Advances in Cardiovascular Disease;Vol. 2 (4), pp. 261-275. 2008eng
dc.rightsDerechos Reservados - Therapeutic Advances in Cardiovascular Disease, 2008spa
dc.rights.accessrightsinfo:eu-repo/semantics/openAccessspa
dc.rights.creativecommonsAtribución-NoComercial 4.0 Internacional (CC BY-NC 4.0)spa
dc.rights.urihttps://creativecommons.org/licenses/by-nc/4.0/spa
dc.sourcehttps://journals.sagepub.com/doi/pdf/10.1177/1753944708092277eng
dc.subject.proposalPreeclampsiaeng
dc.subject.proposalEndotheliumeng
dc.subject.proposalNitric oxideeng
dc.subject.proposalInflammationeng
dc.subject.proposalInfectioneng
dc.titleThe role of the L-arginine-nitric oxide pathway in preeclampsiaeng
dc.typeArtículo de revistaspa
dc.type.coarhttp://purl.org/coar/resource_type/c_6501spa
dc.type.contentTextspa
dc.type.driverinfo:eu-repo/semantics/articlespa
dc.type.redcolhttp://purl.org/redcol/resource_type/ARTspa
dc.type.versioninfo:eu-repo/semantics/publishedVersionspa
dspace.entity.typePublication
oaire.accessrightshttp://purl.org/coar/access_right/c_abf2spa
oaire.versionhttp://purl.org/coar/version/c_970fb48d4fbd8a85spa
Archivos
Paquete original
Mostrando 1 - 1 de 1
Imagen en miniatura
Nombre:
The role of the L-arginine-nitric oxide pathway in preeclampsia.pdf
Tamaño:
289.53 KB
Formato:
Adobe Portable Document Format
Descripción:
Paquete de licencias
Mostrando 1 - 1 de 1
No hay miniatura disponible
Nombre:
license.txt
Tamaño:
59 B
Formato:
Item-specific license agreed upon to submission
Descripción: