dc.creator | Salsoso Rodríguez, Rocío | |
dc.creator | Guzmán Gutiérrez, Enrique | |
dc.creator | Arroyo Zúñiga, Pablo | |
dc.creator | Salomón Gallo, Carlos | |
dc.creator | Zambrano Sevilla, Sonia | |
dc.creator | Ruiz Armenta, María Victoria | |
dc.creator | Blanca Lobato, Antonio Jesús | |
dc.creator | Pardo, Fabián | |
dc.creator | Leiva Mendoza, Andrea | |
dc.creator | Mate Barrero, Alfonso | |
dc.creator | Sobrevia Luarte, Luis | |
dc.creator | Vázquez Cueto, Carmen María | |
dc.date.accessioned | 2015-09-23T11:43:47Z | |
dc.date.available | 2015-09-23T11:43:47Z | |
dc.date.issued | 2014 | |
dc.identifier.citation | Salsoso Rodríguez, R., Guzmán Gutiérrez, E., Arroyo Zúñiga, P., Salomón Gallo, C., Zambrano Sevilla, S., Ruiz Armenta, M.V.,...,Vázquez Cueto, C.M. (2014). Reduced L-carnitine transport in aortic endothelial cells from spontaneously hypertensive rats. Plos One, 9 (2), e90339-1-e90339-11. | |
dc.identifier.issn | 1932-6203 | es |
dc.identifier.uri | http://hdl.handle.net/11441/28768 | |
dc.description.abstract | Impaired L-carnitine uptake correlates with higher blood pressure in adult men, and L-carnitine restores endothelial function in aortic rings from spontaneously hypertensive rat (SHR). Thus, endothelial dysfunction in hypertension could result from lower L-carnitine transport in this cell type. L-Carnitine transport is mainly mediated by novel organic cation transporters 1 (Octn1, Na+-independent) and 2 (Octn2, Na+-dependent); however, their kinetic properties and potential consequences in hypertension are unknown. We hypothesize that L-carnitine transport kinetic properties will be altered in aortic endothelium from spontaneously hypertensive rats (SHR). L-Carnitine transport was measured at different extracellular pH (pHo 5.5–8.5) in the absence or presence of sodium in rat aortic endothelial cells (RAECs) from non-hypertensive Wistar-Kyoto (WKY) rats and SHR. Octn1 and Octn2 mRNA relative expression was also determined. Dilation of endothelium-intact or denuded aortic rings in response to calcitonine gene related peptide (CGRP, 0.1–100 nmol/L) was measured (myography) in the absence or presence of L-carnitine. Total L-carnitine transport was lower in cells from SHR compared with WKY rats, an effect due to reduced Na+-dependent (Na+dep) compared with Na+-independent (Na+indep) transport components. Saturable L-carnitine transport kinetics show maximal velocity (Vmax), without changes in apparent Km for Na+indep transport in SHR compared with WKY rats. Total and Na+dep component of transport were increased, but Na+indep transport was reduced by extracellular alkalization in WKY rats. However, alkalization reduced total and Na+indep transport in cells from SHR. Octn2 mRNA was higher than Octn-1 mRNA expression in cells from both conditions. Dilation of artery rings in response to CGRP was reduced in vessels from SHR compared with WKY rats. CGRP effect was endothelium-dependent and restored by L-carnitine. All together these results suggest that reduced L-carnitine transport (likely via Na+-dependent Octn2) could limit this compound's potential beneficial effects in RAECs from SHR. | es |
dc.format | application/pdf | es |
dc.language.iso | eng | es |
dc.publisher | Public Library of Science | es |
dc.relation.ispartof | Plos One, 9 (2), e90339-1-e90339-11. | |
dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.title | Reduced L-carnitine transport in aortic endothelial cells from spontaneously hypertensive rats | es |
dc.type | info:eu-repo/semantics/article | es |
dcterms.identifier | https://ror.org/03yxnpp24 | |
dc.type.version | info:eu-repo/semantics/publishedVersion | |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | es |
dc.contributor.affiliation | Universidad de Sevilla. Departamento de Fisiología | es |
dc.relation.publisherversion | http://dx.doi.org/10.1371/journal.pone.0090339 | es |
dc.identifier.doi | http://dx.doi.org/10.1371/journal.pone.0090339 | es |
dc.journaltitle | Plos One | es |
dc.publication.volumen | 9 | es |
dc.publication.issue | 2 | es |
dc.publication.initialPage | e90339-1 | es |
dc.publication.endPage | e90339-11 | es |
dc.identifier.idus | https://idus.us.es/xmlui/handle/11441/28768 | |