Full metadata record
DC Field | Value | Language |
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dc.creator | Rodriguez, A. (Amaia) | - |
dc.creator | Frühbeck, G. (Gema) | - |
dc.creator | Gomez-Ambrosi, J. (Javier) | - |
dc.creator | Catalan, V. (Victoria) | - |
dc.creator | Sainz, N. (Neira) | - |
dc.creator | Diez-Martinez, J. (Javier) | - |
dc.creator | Zalba, G. (Guillermo) | - |
dc.creator | Fortuño, A. (Ana) | - |
dc.date.accessioned | 2011-06-20T10:54:34Z | - |
dc.date.available | 2011-06-20T10:54:34Z | - |
dc.date.issued | 2006 | - |
dc.identifier.citation | Rodriguez A, Fruhbeck G, Gomez-Ambrosi J, Catalan V, Sainz N, Diez J, et al. The inhibitory effect of leptin on angiotensin II-induced vasoconstriction is blunted in spontaneously hypertensive rats. J Hypertens 2006 Aug;24(8):1589-1597. | es_ES |
dc.identifier.issn | 1473-5598 | - |
dc.identifier.uri | https://hdl.handle.net/10171/18589 | - |
dc.description.abstract | OBJECTIVE: Leptin attenuates the angiotensin II-induced increase of cytosolic calcium ([Ca2+]i) and vasoconstriction in the aorta of normotensive Wistar rats. To determine whether these effects may be altered in hypertension, we assessed the effect of leptin on angiotensin II-induced vascular response in the aorta of 10-week-old spontaneously hypertensive rats (SHR). METHODS: Contractile responses to angiotensin II (100 nmol/l) in the presence of different concentrations of leptin (0.1, 1, 10, 100 nmol/l) were evaluated in isolated aortic rings by the organ bath system. [Ca2+]i was measured in vascular smooth muscle cells (VSMCs) using Fura-2 fluorescence. The expression of the short (OB-Ra) and long (OB-Rb) isoforms of the leptin receptor in VSMCs was evaluated by real-time reverse transcriptase-polymerase chain reaction and western-blot analysis. RESULTS: Circulating leptin concentrations were increased in SHR. Serum metabolic parameters, including glucose, insulin, total cholesterol and triglyceride levels, were also elevated in SHR. Leptin did not modify the angiotensin II-induced vasoconstriction in SHR either in intact or endothelium-denuded aortic rings. In addition, leptin was not able either to diminish the angiotensin II-induced the peak rise of [Ca2+]i or to accelerate the recovery rate to basal calcium levels in VSMCs from SHR. However, OB-Ra and OB-Rb mRNA and protein expression were increased in SHR VSMCs. CONCLUSIONS: The lack of effect of leptin on angiotensin II-induced contraction in the aorta of SHR is due to an impaired handling of [Ca2+]i in VSMCs. Hyperleptinemia and overexpression of OB-R in VSMCs could be compensatory mechanisms against VSMC leptin resistance in genetically hypertensive rats. | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Lippincott, Williams & Wilkins | es_ES |
dc.rights | info:eu-repo/semantics/closedAccess | - |
dc.subject | Leptin | es_ES |
dc.subject | Angiotensin | es_ES |
dc.subject | Hypertension | es_ES |
dc.subject | Obesity | es_ES |
dc.subject | Smooth muscle | es_ES |
dc.subject | Calcium | es_ES |
dc.title | The inhibitory effect of leptin on angiotensin II-induced vasoconstriction is blunted in spontaneously hypertensive rats | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.relation.publisherversion | http://bit.ly/kNGL8G | es_ES |
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