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Título: | Mechanisms underlying the activation of L-type calcium channels by urocortin in rat ventricular myocytes |
Autor: | Smani, Tarik CSIC ORCID; Calderón-Sánchez, Eva CSIC; Gómez-Hurtado, Nieves; Fernández-Velasco, María CSIC ORCID; Cachofeiro, Victoria; Ordóñez Fernández, Antonio CSIC ORCID; Delgado, Carmen CSIC ORCID | Palabras clave: | Urocortin L-type calcium channels Patch-clamp PKC ERK1/2 |
Fecha de publicación: | 2010 | Editor: | Oxford University Press European Society of Cardiology |
Citación: | Cardiovascular Research 87(3): 459-466 (2010) | Resumen: | [Aims]: The aim of this study was to elucidate the signalling pathways implicated in the modulation of cardiac L-type Ca2+ channels by urocortin (Ucn) in ventricular myocytes. [Methods and results]: Adult rat ventricular myocytes were stimulated in vitro with Ucn for 20–40 min. L-type calcium currents (ICaL) were measured with the patch-clamp technique, whereas quantification of activation of extracellular signal-regulated kinases 1/2 (ERK1/2) was assessed by sandwich-ELISA. Ucn induced a significant increase in ICaL density that was not prevented by the protein kinase A (PKA) inhibitor KT-5720 or the non-selective antagonist of guanine nucleotide exchange factor brefeldin A. The Ucn effect was antagonized by astressin, a corticotropin-releasing factor receptor-2 (CRF-R2) antagonist, and significantly reduced by protein kinase C (PKC) and ERK1/2 inhibitors. The cyclic AMP (cAMP) analogue 8-pCPT-2′OMe-cAMP, which selectively activates the exchange protein activated by cAMP (Epac), was ineffective in modifying ICaL. Analysis of phospho-ERK1/2 showed that Ucn induced a significant activation of the ERK1/2 pathway in ventricular myocytes and this effect was prevented by pre-incubation with PKC inhibitors. [Conclusion]: The present study provides evidence of new mechanisms involved in the modulation of L-type Ca2+ channels by Ucn in adult ventricular myocytes. We propose that the marked increase in ICaL density induced by Ucn is mediated through CRF-R2 and involves PKC-dependent activation of the ERK1/2 pathway, whereas PKA and Epac signalling are not implicated. | Descripción: | 8 páginas, 7 figuras. | Versión del editor: | http://dx.doi.org/10.1093/cvr/cvq063 | URI: | http://hdl.handle.net/10261/42360 | DOI: | 10.1093/cvr/cvq063 | ISSN: | 0008-6363 | E-ISSN: | 1755-3245 |
Aparece en las colecciones: | (CIB) Artículos (IBIS) Artículos |
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