Mañana, JUEVES, 24 DE ABRIL, el sistema se apagará debido a tareas habituales de mantenimiento a partir de las 9 de la mañana. Lamentamos las molestias.
Anticontractile effect of perivascular adipose tissue and leptin are reduced in hypertension
Author
Gálvez-Prieto, Beatriz; Somoza, Beatriz; Gil-Ortega, Marta; García-Prieto, Concha F.; De Las Heras, Ana Isabel; González Enguita, María del Carmen; Arribas Rodríguez, Silvia Magdalena; Aránguez, Isabel; Bolbrinker, Juliane; Kreutz, Reinhold; Ruiz-Gayo, Mariano; Fernández-Alfonso, María SoledadEntity
UAM. Departamento de FisiologíaPublisher
FrontiersDate
2012Citation
10.3389/fphar.2012.00103
Frontiers in pharmacology 3 (2012): 103
ISSN
1663-9812 (online)DOI
10.3389/fphar.2012.00103Funded by
This work was supported by grants from Ministerio de Educación y Ciencia (SAF 2009-09714, SAF2008-02703), Grupos UCM GR-921641, Fundación Universitaria San Pablo-CEU, Fundación Mutua Madrileña, and SESCAMETEditor's Version
http://dx.doi.org/10.3389/fphar.2012.00103Subjects
Angiotensin II; Hypertension; Leptin; Nitric oxide; Perivascular adipose tissue; MedicinaRights
© 2012 Los autoresAbstract
Leptin causes vasodilatation both by endothelium-dependent and -independent mechanisms. Leptin is synthesized by perivascular adipose tissue (PVAT). The hypothesis of this study is that a decrease of leptin production in PVAT of spontaneously hypertensive rats (SHR) might contribute to a diminished paracrine anticontractile effect of the hormone. We have determined in aorta from Wistar-Kyoto (WKY) and SHR (i) leptin mRNA and protein levels in PVAT, (ii) the effect of leptin and PVAT on contractile responses, and (iii) leptin-induced relaxation and nitric oxide (NO) production. Leptin mRNA and protein expression were significantly lower in PVAT from SHR. Concentration-response curves to angiotensin II were significantly blunted in presence of PVAT as well as by exogenous leptin (10−9 M) only in WKY. This anticontractile effect was endothelium-dependent. Vasodilatation induced by leptin was smaller in SHR than in WKY, and was also endothelium-dependent. Moreover, release of endothelial NO in response to acute leptin was higher in WKY compared to SHR, but completely abolished in the absence of endothelium. In conclusion, the reduced anticontractile effect of PVAT in SHR might be attributed to a reduced PVAT-derived leptin and to an abrogated effect of leptin on endothelial NO release probably due to an impaired activation of endothelial NO synthase.
Files in this item
Google Scholar:Gálvez-Prieto, Beatriz
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Somoza, Beatriz
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Gil-Ortega, Marta
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García-Prieto, Concha F.
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De Las Heras, Ana Isabel
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González Enguita, María del Carmen
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Arribas Rodríguez, Silvia Magdalena
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Aránguez, Isabel
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Bolbrinker, Juliane
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Kreutz, Reinhold
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Ruiz-Gayo, Mariano
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Fernández-Alfonso, María Soledad
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