Please use this identifier to cite or link to this item: http://hdl.handle.net/10637/14615

Anticontractile Effect of Perivascular Adipose Tissue and Leptin are Reduced in Hypertension

Title: Anticontractile Effect of Perivascular Adipose Tissue and Leptin are Reduced in Hypertension
Authors : Gálvez-Prieto, Beatriz
Somoza Hernández, Beatriz
Gil Ortega, Marta
García Prieto, Concepción F.
De las Heras, Ana I.
González, María del Carmen
Arribas Rodríguez, Silvia Magdalena
Aránguez, Isabel
Bolbrinker, Juliane
Kreutz, Reinhold
Ruíz Gayo, Mariano
Fernández Alfonso, María Soledad
Keywords: Perivascular adipose tissueHypertensionAngiotensin IILeptin
Citation: Gálvez-Prieto B, Somoza B, Gil-Ortega M, García-Prieto CF, de Las Heras AI, González MC, Arribas S, Aranguez I, Bolbrinker J, Kreutz R, Ruiz-Gayo M, Fernández-Alfonso MS. Anticontractile Effect of Perivascular Adipose Tissue and Leptin are Reduced in Hypertension. Front Pharmacol. 2012 Jun 5;3:103. doi: 10.3389/fphar.2012.00103
Abstract: 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 adiminished paracrine anticontractile effect of the hormone. We have determined in aorta from Wistar-Kyoto (WKY) and SHR leptin mRNA and protein levels in PVAT, the effect of leptin and PVAT on contractile responses, and leptin-induced relaxation and nitricoxide (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 exogenousleptin (10−9M) 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. More over, release of endothelial NO in response to acute leptin was higherin 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
URI: http://hdl.handle.net/10637/14615
Rights : http://creativecommons.org/licenses/by-nc-nd/4.0/deed.es
OpenAccess
ISSN: 1663-9812
Issue Date: 5-Jun-2012
Center : Universidad San Pablo-CEU
Appears in Collections:Facultad de Farmacia





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