Fetoplacental endothelial dysfunction in maternal hypercholesterolemia and obesity in pregnancy

Autores
Pardo, Fabián; Silva, Luis; Salsoso, Rocío; Sáez, Tamara; Farías, Marcelo; Villalobos, Roberto; Leiva, Andrea; Sanhueza, Carlos; Sobrevia, Luis
Año de publicación
2014
Idioma
inglés
Tipo de recurso
reseña artículo
Estado
versión publicada
Descripción
Human fetoplacental vascular function is altered in several pathologies of pregnancy as a result of endothelial dysfunction. Pregnancy is a physiological condition coursing with increased circulating plasma levels of cholesterol in the mother, to respond to the higher demands from the growing fetus. An abnormal increase in maternal plasma cholesterol configures a pathological state referred as maternal supraphysiological hypercholesterolemia (MSPH). In MSPH, L-arginine transport and synthesis of nitric oxide (i.e., L-arginine/NO signalling pathway) as well as arginases/urea cycle in the fetoplacental endothelium are altered. Equally, an increase in the physiological gain of weight in pregnant women could end with obese women at the end of pregnancy leading to a condition referred as obesity in pregnancy (OP). OP seems to be also associated with alterations in the L-arginine/NO signalling pathway in endothelium in animal models; however, nothing is known regarding alterations of the human fetoplacental endothelium in OP. Insulin, adenosine and NO are vasodilators in the fetoplacental vascular bed, and a role for these molecules is proposed in MSPH and OP. Alternatively, involvement of intracellular pH modulation and the potential involvement of adenosine receptors is proposed as phenomena that could improve endothelial dysfunction associated with these diseases of pregnancy.
Sociedad Argentina de Fisiología
Materia
Ciencias Médicas
Endothelial dysfunction
Pregnancy
Nivel de accesibilidad
acceso abierto
Condiciones de uso
http://creativecommons.org/licenses/by/4.0/
Repositorio
SEDICI (UNLP)
Institución
Universidad Nacional de La Plata
OAI Identificador
oai:sedici.unlp.edu.ar:10915/125642

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network_name_str SEDICI (UNLP)
spelling Fetoplacental endothelial dysfunction in maternal hypercholesterolemia and obesity in pregnancyPardo, FabiánSilva, LuisSalsoso, RocíoSáez, TamaraFarías, MarceloVillalobos, RobertoLeiva, AndreaSanhueza, CarlosSobrevia, LuisCiencias MédicasEndothelial dysfunctionPregnancyHuman fetoplacental vascular function is altered in several pathologies of pregnancy as a result of endothelial dysfunction. Pregnancy is a physiological condition coursing with increased circulating plasma levels of cholesterol in the mother, to respond to the higher demands from the growing fetus. An abnormal increase in maternal plasma cholesterol configures a pathological state referred as maternal supraphysiological hypercholesterolemia (MSPH). In MSPH, L-arginine transport and synthesis of nitric oxide (i.e., L-arginine/NO signalling pathway) as well as arginases/urea cycle in the fetoplacental endothelium are altered. Equally, an increase in the physiological gain of weight in pregnant women could end with obese women at the end of pregnancy leading to a condition referred as obesity in pregnancy (OP). OP seems to be also associated with alterations in the L-arginine/NO signalling pathway in endothelium in animal models; however, nothing is known regarding alterations of the human fetoplacental endothelium in OP. Insulin, adenosine and NO are vasodilators in the fetoplacental vascular bed, and a role for these molecules is proposed in MSPH and OP. Alternatively, involvement of intracellular pH modulation and the potential involvement of adenosine receptors is proposed as phenomena that could improve endothelial dysfunction associated with these diseases of pregnancy.Sociedad Argentina de Fisiología2014-10info:eu-repo/semantics/reviewinfo:eu-repo/semantics/publishedVersionRevisionhttp://purl.org/coar/resource_type/c_dcae04bcinfo:ar-repo/semantics/resenaArticuloapplication/pdf60-76http://sedici.unlp.edu.ar/handle/10915/125642enginfo:eu-repo/semantics/altIdentifier/url/https://pmr.safisiol.org.ar/archive/id/67info:eu-repo/semantics/altIdentifier/issn/1669-5402info:eu-repo/semantics/altIdentifier/issn/1669-5410info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by/4.0/Creative Commons Attribution 4.0 International (CC BY 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-09-29T11:30:13Zoai:sedici.unlp.edu.ar:10915/125642Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-29 11:30:13.349SEDICI (UNLP) - Universidad Nacional de La Platafalse
dc.title.none.fl_str_mv Fetoplacental endothelial dysfunction in maternal hypercholesterolemia and obesity in pregnancy
title Fetoplacental endothelial dysfunction in maternal hypercholesterolemia and obesity in pregnancy
spellingShingle Fetoplacental endothelial dysfunction in maternal hypercholesterolemia and obesity in pregnancy
Pardo, Fabián
Ciencias Médicas
Endothelial dysfunction
Pregnancy
title_short Fetoplacental endothelial dysfunction in maternal hypercholesterolemia and obesity in pregnancy
title_full Fetoplacental endothelial dysfunction in maternal hypercholesterolemia and obesity in pregnancy
title_fullStr Fetoplacental endothelial dysfunction in maternal hypercholesterolemia and obesity in pregnancy
title_full_unstemmed Fetoplacental endothelial dysfunction in maternal hypercholesterolemia and obesity in pregnancy
title_sort Fetoplacental endothelial dysfunction in maternal hypercholesterolemia and obesity in pregnancy
dc.creator.none.fl_str_mv Pardo, Fabián
Silva, Luis
Salsoso, Rocío
Sáez, Tamara
Farías, Marcelo
Villalobos, Roberto
Leiva, Andrea
Sanhueza, Carlos
Sobrevia, Luis
author Pardo, Fabián
author_facet Pardo, Fabián
Silva, Luis
Salsoso, Rocío
Sáez, Tamara
Farías, Marcelo
Villalobos, Roberto
Leiva, Andrea
Sanhueza, Carlos
Sobrevia, Luis
author_role author
author2 Silva, Luis
Salsoso, Rocío
Sáez, Tamara
Farías, Marcelo
Villalobos, Roberto
Leiva, Andrea
Sanhueza, Carlos
Sobrevia, Luis
author2_role author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Ciencias Médicas
Endothelial dysfunction
Pregnancy
topic Ciencias Médicas
Endothelial dysfunction
Pregnancy
dc.description.none.fl_txt_mv Human fetoplacental vascular function is altered in several pathologies of pregnancy as a result of endothelial dysfunction. Pregnancy is a physiological condition coursing with increased circulating plasma levels of cholesterol in the mother, to respond to the higher demands from the growing fetus. An abnormal increase in maternal plasma cholesterol configures a pathological state referred as maternal supraphysiological hypercholesterolemia (MSPH). In MSPH, L-arginine transport and synthesis of nitric oxide (i.e., L-arginine/NO signalling pathway) as well as arginases/urea cycle in the fetoplacental endothelium are altered. Equally, an increase in the physiological gain of weight in pregnant women could end with obese women at the end of pregnancy leading to a condition referred as obesity in pregnancy (OP). OP seems to be also associated with alterations in the L-arginine/NO signalling pathway in endothelium in animal models; however, nothing is known regarding alterations of the human fetoplacental endothelium in OP. Insulin, adenosine and NO are vasodilators in the fetoplacental vascular bed, and a role for these molecules is proposed in MSPH and OP. Alternatively, involvement of intracellular pH modulation and the potential involvement of adenosine receptors is proposed as phenomena that could improve endothelial dysfunction associated with these diseases of pregnancy.
Sociedad Argentina de Fisiología
description Human fetoplacental vascular function is altered in several pathologies of pregnancy as a result of endothelial dysfunction. Pregnancy is a physiological condition coursing with increased circulating plasma levels of cholesterol in the mother, to respond to the higher demands from the growing fetus. An abnormal increase in maternal plasma cholesterol configures a pathological state referred as maternal supraphysiological hypercholesterolemia (MSPH). In MSPH, L-arginine transport and synthesis of nitric oxide (i.e., L-arginine/NO signalling pathway) as well as arginases/urea cycle in the fetoplacental endothelium are altered. Equally, an increase in the physiological gain of weight in pregnant women could end with obese women at the end of pregnancy leading to a condition referred as obesity in pregnancy (OP). OP seems to be also associated with alterations in the L-arginine/NO signalling pathway in endothelium in animal models; however, nothing is known regarding alterations of the human fetoplacental endothelium in OP. Insulin, adenosine and NO are vasodilators in the fetoplacental vascular bed, and a role for these molecules is proposed in MSPH and OP. Alternatively, involvement of intracellular pH modulation and the potential involvement of adenosine receptors is proposed as phenomena that could improve endothelial dysfunction associated with these diseases of pregnancy.
publishDate 2014
dc.date.none.fl_str_mv 2014-10
dc.type.none.fl_str_mv info:eu-repo/semantics/review
info:eu-repo/semantics/publishedVersion
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format review
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dc.identifier.none.fl_str_mv http://sedici.unlp.edu.ar/handle/10915/125642
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dc.language.none.fl_str_mv eng
language eng
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info:eu-repo/semantics/altIdentifier/issn/1669-5402
info:eu-repo/semantics/altIdentifier/issn/1669-5410
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by/4.0/
Creative Commons Attribution 4.0 International (CC BY 4.0)
eu_rights_str_mv openAccess
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Creative Commons Attribution 4.0 International (CC BY 4.0)
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instname:Universidad Nacional de La Plata
instacron:UNLP
reponame_str SEDICI (UNLP)
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instname_str Universidad Nacional de La Plata
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repository.name.fl_str_mv SEDICI (UNLP) - Universidad Nacional de La Plata
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