Arginine NO-dependent and NO-independent effects on hemodynamics

Autores
Guridi, Jorge; Borgatello, Conrado; Scremin, Oscar Umberto
Año de publicación
2014
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
L-arginine administration decreases mean arterial blood pressure (MABP), presumably by excess nitric oxide (NO) synthesis. However, some reports indicate that D-arginine, not a substrate of NO synthase (NOS), also induces hypotension. To clarify this phenomenon, the hemodynamic effects of L- and D-arginine and their modification by NOS inhibition with L-nitroarginine methyl ester (L-NAME) were assessed. MABP, cardiac output, stroke volume, heart rate and systemic vascular resistance were recorded in Sprague-Dawley rats under urethane or ketamine/diazepam anesthesia, with or without blockade of NO synthesis by L-NAME. Both stereoisomers of arginine induced a dose-related drop in MABP of similar magnitude and time course, but recovery from hypotension was slower in L-arginine than in D-arginine. The hypotension induced by both stereoisomers was due to a decrease in systemic vascular resistance (SVR) with increase in cardiac output (CO) and stroke volume (SV). Administration of L-NAME induced a pronounced increase in MABP and SVR, with decreases in CO and heart rate (HR). Infusion of L-arginine after L-NAME significantly decreased MABP and SVR at the highest dose while D-arginine failed to do so. After L-NAME, MABP was significantly lower under L-arginine than under D-arginine at all doses. These experiments suggest a dual mechanism in the hypotensive effect of L-arginine: a NO independent action on vascular resistance shared with D-arginine, and a NO dependent mechanism that becomes evident in the presence of NOS inhibition with L-NAME. Cardiac effects of NO do not appear to play a role in Larginine hypotension
Fil: Guridi, Jorge. Universidad Nacional de Rosario. Facultad de Ciencias Médicas; Argentina
Fil: Borgatello, Conrado. Universidad Nacional de Rosario; Argentina
Fil: Scremin, Oscar Umberto. Universidad Nacional de Rosario; Argentina. Greater Los Angeles Healthcare System. Los Angeles; Estados Unidos. David Geffen School of Medicine at UCLA; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Materia
L-Name
Nitric Oxide Synthase
Arterial Blood Pressure
Cardiac Output
Systemic Vascular Resistance
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/29905

id CONICETDig_a612c440962f9b0aca698eb75d82a9d0
oai_identifier_str oai:ri.conicet.gov.ar:11336/29905
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Arginine NO-dependent and NO-independent effects on hemodynamicsGuridi, JorgeBorgatello, ConradoScremin, Oscar UmbertoL-NameNitric Oxide SynthaseArterial Blood PressureCardiac OutputSystemic Vascular Resistancehttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1L-arginine administration decreases mean arterial blood pressure (MABP), presumably by excess nitric oxide (NO) synthesis. However, some reports indicate that D-arginine, not a substrate of NO synthase (NOS), also induces hypotension. To clarify this phenomenon, the hemodynamic effects of L- and D-arginine and their modification by NOS inhibition with L-nitroarginine methyl ester (L-NAME) were assessed. MABP, cardiac output, stroke volume, heart rate and systemic vascular resistance were recorded in Sprague-Dawley rats under urethane or ketamine/diazepam anesthesia, with or without blockade of NO synthesis by L-NAME. Both stereoisomers of arginine induced a dose-related drop in MABP of similar magnitude and time course, but recovery from hypotension was slower in L-arginine than in D-arginine. The hypotension induced by both stereoisomers was due to a decrease in systemic vascular resistance (SVR) with increase in cardiac output (CO) and stroke volume (SV). Administration of L-NAME induced a pronounced increase in MABP and SVR, with decreases in CO and heart rate (HR). Infusion of L-arginine after L-NAME significantly decreased MABP and SVR at the highest dose while D-arginine failed to do so. After L-NAME, MABP was significantly lower under L-arginine than under D-arginine at all doses. These experiments suggest a dual mechanism in the hypotensive effect of L-arginine: a NO independent action on vascular resistance shared with D-arginine, and a NO dependent mechanism that becomes evident in the presence of NOS inhibition with L-NAME. Cardiac effects of NO do not appear to play a role in Larginine hypotensionFil: Guridi, Jorge. Universidad Nacional de Rosario. Facultad de Ciencias Médicas; ArgentinaFil: Borgatello, Conrado. Universidad Nacional de Rosario; ArgentinaFil: Scremin, Oscar Umberto. Universidad Nacional de Rosario; Argentina. Greater Los Angeles Healthcare System. Los Angeles; Estados Unidos. David Geffen School of Medicine at UCLA; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaElsevier Science2014-04info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/29905Guridi, Jorge; Borgatello, Conrado; Scremin, Oscar Umberto; Arginine NO-dependent and NO-independent effects on hemodynamics; Elsevier Science; European Journal of Pharmacology; 729; 4-2014; 138-1430014-2999CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.ejphar.2014.01.070info:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S0014299914001162info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-15T15:21:40Zoai:ri.conicet.gov.ar:11336/29905instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-10-15 15:21:41.187CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Arginine NO-dependent and NO-independent effects on hemodynamics
title Arginine NO-dependent and NO-independent effects on hemodynamics
spellingShingle Arginine NO-dependent and NO-independent effects on hemodynamics
Guridi, Jorge
L-Name
Nitric Oxide Synthase
Arterial Blood Pressure
Cardiac Output
Systemic Vascular Resistance
title_short Arginine NO-dependent and NO-independent effects on hemodynamics
title_full Arginine NO-dependent and NO-independent effects on hemodynamics
title_fullStr Arginine NO-dependent and NO-independent effects on hemodynamics
title_full_unstemmed Arginine NO-dependent and NO-independent effects on hemodynamics
title_sort Arginine NO-dependent and NO-independent effects on hemodynamics
dc.creator.none.fl_str_mv Guridi, Jorge
Borgatello, Conrado
Scremin, Oscar Umberto
author Guridi, Jorge
author_facet Guridi, Jorge
Borgatello, Conrado
Scremin, Oscar Umberto
author_role author
author2 Borgatello, Conrado
Scremin, Oscar Umberto
author2_role author
author
dc.subject.none.fl_str_mv L-Name
Nitric Oxide Synthase
Arterial Blood Pressure
Cardiac Output
Systemic Vascular Resistance
topic L-Name
Nitric Oxide Synthase
Arterial Blood Pressure
Cardiac Output
Systemic Vascular Resistance
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv L-arginine administration decreases mean arterial blood pressure (MABP), presumably by excess nitric oxide (NO) synthesis. However, some reports indicate that D-arginine, not a substrate of NO synthase (NOS), also induces hypotension. To clarify this phenomenon, the hemodynamic effects of L- and D-arginine and their modification by NOS inhibition with L-nitroarginine methyl ester (L-NAME) were assessed. MABP, cardiac output, stroke volume, heart rate and systemic vascular resistance were recorded in Sprague-Dawley rats under urethane or ketamine/diazepam anesthesia, with or without blockade of NO synthesis by L-NAME. Both stereoisomers of arginine induced a dose-related drop in MABP of similar magnitude and time course, but recovery from hypotension was slower in L-arginine than in D-arginine. The hypotension induced by both stereoisomers was due to a decrease in systemic vascular resistance (SVR) with increase in cardiac output (CO) and stroke volume (SV). Administration of L-NAME induced a pronounced increase in MABP and SVR, with decreases in CO and heart rate (HR). Infusion of L-arginine after L-NAME significantly decreased MABP and SVR at the highest dose while D-arginine failed to do so. After L-NAME, MABP was significantly lower under L-arginine than under D-arginine at all doses. These experiments suggest a dual mechanism in the hypotensive effect of L-arginine: a NO independent action on vascular resistance shared with D-arginine, and a NO dependent mechanism that becomes evident in the presence of NOS inhibition with L-NAME. Cardiac effects of NO do not appear to play a role in Larginine hypotension
Fil: Guridi, Jorge. Universidad Nacional de Rosario. Facultad de Ciencias Médicas; Argentina
Fil: Borgatello, Conrado. Universidad Nacional de Rosario; Argentina
Fil: Scremin, Oscar Umberto. Universidad Nacional de Rosario; Argentina. Greater Los Angeles Healthcare System. Los Angeles; Estados Unidos. David Geffen School of Medicine at UCLA; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
description L-arginine administration decreases mean arterial blood pressure (MABP), presumably by excess nitric oxide (NO) synthesis. However, some reports indicate that D-arginine, not a substrate of NO synthase (NOS), also induces hypotension. To clarify this phenomenon, the hemodynamic effects of L- and D-arginine and their modification by NOS inhibition with L-nitroarginine methyl ester (L-NAME) were assessed. MABP, cardiac output, stroke volume, heart rate and systemic vascular resistance were recorded in Sprague-Dawley rats under urethane or ketamine/diazepam anesthesia, with or without blockade of NO synthesis by L-NAME. Both stereoisomers of arginine induced a dose-related drop in MABP of similar magnitude and time course, but recovery from hypotension was slower in L-arginine than in D-arginine. The hypotension induced by both stereoisomers was due to a decrease in systemic vascular resistance (SVR) with increase in cardiac output (CO) and stroke volume (SV). Administration of L-NAME induced a pronounced increase in MABP and SVR, with decreases in CO and heart rate (HR). Infusion of L-arginine after L-NAME significantly decreased MABP and SVR at the highest dose while D-arginine failed to do so. After L-NAME, MABP was significantly lower under L-arginine than under D-arginine at all doses. These experiments suggest a dual mechanism in the hypotensive effect of L-arginine: a NO independent action on vascular resistance shared with D-arginine, and a NO dependent mechanism that becomes evident in the presence of NOS inhibition with L-NAME. Cardiac effects of NO do not appear to play a role in Larginine hypotension
publishDate 2014
dc.date.none.fl_str_mv 2014-04
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/29905
Guridi, Jorge; Borgatello, Conrado; Scremin, Oscar Umberto; Arginine NO-dependent and NO-independent effects on hemodynamics; Elsevier Science; European Journal of Pharmacology; 729; 4-2014; 138-143
0014-2999
CONICET Digital
CONICET
url http://hdl.handle.net/11336/29905
identifier_str_mv Guridi, Jorge; Borgatello, Conrado; Scremin, Oscar Umberto; Arginine NO-dependent and NO-independent effects on hemodynamics; Elsevier Science; European Journal of Pharmacology; 729; 4-2014; 138-143
0014-2999
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1016/j.ejphar.2014.01.070
info:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S0014299914001162
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Elsevier Science
publisher.none.fl_str_mv Elsevier Science
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
_version_ 1846083364480614400
score 12.891075