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dc.date.accessioned 2019-10-29T14:15:06Z
dc.date.available 2019-10-29T14:15:06Z
dc.date.issued 2005
dc.identifier.uri https://sedici.unlp.edu.ar/handle/10915/84302
dc.description.abstract This study aimed to explore the signaling pathways involved in the positive inotropic effect (PIE) of low doses of endothelin-1 (ET-1). Cat papillary muscles were used for force and intracellular Na+ concentration (Na+i) measurements, and isolated cat ventricular myocytes for patch-clamp experiments. ET-1 (5 nmol/L) induced a PIE and an associated increase in Na+i that were abolished by Na +/H+ exchanger (NHE) inhibition with HOE642. Reverse-mode Na+/Ca2+ exchanger (NCX) blockade with KB-R7943 reversed the ET-1-induced PIE. These results suggest that the ET-1-induced PIE is totally attributable to the NHE-mediated Na+i increase. However, an additional direct stimulating effect of ET-1 on NCX after the necessary increase in Na+i could occur. Thus, the ET-1-induced increase in Na+i and contractility was compared with that induced by partial inhibition of the Na+/K+ ATPase by lowering extracellular K+ (K+o) For a given Na+i, ET-1 induced a greater PIE than low K+o. In the presence of HOE642 and after increasing contractility and Na+i by low K+o, ET-1 induced an additional PIE that was reversed by KB-R7943 or the protein kinase C (PKC) inhibitor chelerythrine. ET-1 increased the NCX current and negatively shifted the NCX reversal potential (ENCX). HOE642 attenuated the increase in NCX outward current and abolished the ENCX shift. These results indicate that whereas the NHE-mediated ET-1-induced increase in Na+i seems to be mandatory to drive NCX in reverse and enhance contractility, Na+i-independent and PKC-dependent NCX stimulation appears to additionally contribute to the PIE. However, it is important to stress that the latter can only occur after the primary participation of the former. en
dc.format.extent 288-293 es
dc.language en es
dc.subject Contraction es
dc.subject Endothelin es
dc.subject Ion channels es
dc.title Endothelin-1 stimulates the Na+/Ca2+ exchanger reverse mode through intracellular Na+ (Na+i) - Dependent and Na+i-independent pathways en
dc.type Articulo es
sedici.identifier.other doi:10.1161/01.HYP.0000152700.58940.b2 es
sedici.identifier.other eid:2-s2.0-13144261662 es
sedici.identifier.issn 0194-911X es
sedici.creator.person Aiello, Ernesto Alejandro es
sedici.creator.person Villa Abrille, María Celeste es
sedici.creator.person Dulce, Raúl Ariel es
sedici.creator.person Cingolani, Horacio Eugenio es
sedici.creator.person Pérez, Néstor Gustavo es
sedici.subject.materias Ciencias Médicas es
sedici.description.fulltext true es
mods.originInfo.place Facultad de Ciencias Médicas es
mods.originInfo.place Centro de Investigaciones Cardiovasculares es
sedici.subtype Articulo es
sedici.rights.license Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)
sedici.rights.uri http://creativecommons.org/licenses/by-nc-sa/4.0/
sedici.description.peerReview peer-review es
sedici.relation.journalTitle Hypertension es
sedici.relation.journalVolumeAndIssue vol. 45, no. 2 es
sedici.rights.sherpa * RoMEO: amarillo* Pre-print del autor: can* Post-print del autor: restricted* Versión de editor/PDF:cannot* Condiciones:>>Author's pre-print on pre-print server only>>Must inform publisher of any pre-print deposit>>Author's pre-print must not be updated with future versions>>Author's post-print on Institutional repository or funding agency repository>>En un servidor sin ánimo de lucro>>La versión de editor/PDF no puede utilizarse>>Publisher will automatically deposit authors post-print in PubMed Central for NIH funded authors after 12 months>>Publisher will automatically deposit authors post-print in PubMed Central for HHMI and Wellcome Trust funded authors after 6 months>>Authors may place a 'toll-free' link to their article on authors' personal website or institutional website without embargo>>Debe enlazar a la versión de editor con DOI>>Publisher last contacted on 07/06/2018* Link a Sherpa: http://sherpa.ac.uk/romeo/issn/0194-911X/es/


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Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) Except where otherwise noted, this item's license is described as Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)